Link between viral infection, specialized lung cells and COPD

Main Category: COPD
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 20 Aug 2013 - 1:00 PDT Current ratings for:
Link between viral infection, specialized lung cells and COPD

Investigators at Washington University School of Medicine in St. Louis have described another link in the chain of events that connect acute viral infections to the development of chronic obstructive pulmonary disease (COPD). Their discovery points to a new therapeutic target for COPD, an extremely common disease of the lower airways that is seen in chronic bronchitis and emphysema.

COPD affects about 12 million people in the United States, where it is the third leading cause of death. Worldwide, it is the fifth leading cause of death. It is characterized by inflammation of the lower airways and destruction of lung tissue that limit airflow and pulmonary function. No effective treatments exist to specifically address a major cause of disease advancement and death from COPD - excess inflammatory mucus that blocks airways and prevents normal breathing.

It is well established that smoke exposure is a major risk factor for COPD, but in this new research, investigators show that the cells that line the airways also can respond to viruses in a way that leads to long-term lung inflammation and mucus production that are typical of COPD.

The research, featured on the cover of the September issue of the Journal of Clinical Investigation, reconciles the discrepancy between the transient nature of most viral infections and the relatively permanent nature of chronic inflammatory diseases such as COPD.

Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine at Washington University, has devoted much of his career to understanding the connections between environmental agents and development of chronic lung disease. Five years ago, he and his colleagues reported that a signaling molecule called interleukin-13 (IL-13) was the key driver of excess production of chronic airway mucus after viral infection. Since then, they have pursued the basis for IL-13 production and its usefulness as a marker and a target for more precise therapeutic intervention in COPD and related diseases such as asthma.

The team traced the source of IL-13 to the immune cells of the innate immune system that had not previously been described as part of COPD. But until now, they didn't know how this type of immune response could be perpetuated to cause such a long-term disease like COPD.

"The innate immune response is conventionally viewed as built for short- rather than long-term activation," said Holtzman. "So the type of pathway that we identified was thought to be activated for only short periods of time. However, we found that it could be persistently activated after viral infection and became even more active with time."

The new research identifies another signaling molecule that plays a key role in this phenomenon.

"We reasoned that events upstream from IL-13 production might be involved in keeping the immune response active," said the study's lead author, Derek Byers, PhD, MD, assistant professor of medicine. "When we checked for candidates, we focused our efforts on the types of molecules that are associated with controlling the immune response and especially the production of IL-13."

One of these candidates, a signaling molecule called IL-33, was strongly linked to production of IL-13 in a mouse model of chronic obstructive lung disease that developed after viral infection. In fact, delivery of IL-33 directly to the airway in these animals was also enough to cause production of IL-13 and accumulation of mucus in the lungs.

Working further in this experimental model, co-lead author Jennifer Alexander-Brett, MD, PhD, a postdoctoral fellow, traced the source of the upstream signaling molecule IL-33 to a specialized set of cells within the epithelial layer that lines the airways of the lung. These IL-33-producing epithelial cells were found to possess the characteristics of progenitor cells - meaning that these cells, like stem cells, had the ability to self-renew and to execute a program that gave rise to a complete airway.

"To translate our findings from the mouse model to humans, we used whole lungs removed from patients undergoing lung transplantation for very severe COPD," said Alexander-Brett. Analysis of these human tissue samples also pointed to epithelial cells with progenitor properties as the source of IL-33.

"From this work, we now know that a respiratory viral infection leads to an increase in lung epithelial progenitor cells that are programmed for increased production of IL-33," said Holtzman. "We also provided the initial evidence that an additional stress or danger, such as smoking or pollution or even another infection, could cause these cells to release IL-33, which then stimulates immune cells to produce IL-13 and in turn the airway mucus typical of COPD and related respiratory diseases. It's also possible that smoke exposure predisposes individuals to the development of these cells and, in turn, the susceptibility to exacerbation and progression of this type of disease."

He noted that it is reasonable to think that monitoring the IL-33 to IL-13 pathway will allow physicians to identify which patients would benefit from strategies to interrupt this cascade and prevent an otherwise progressive and devastating respiratory disease.

"This work suggests that previous viral infections of the lung may worsen COPD by stimulating a particular type of lung cell that overactivates the immune system," noted James P. Kiley, PhD, director of the Division of Lung Diseases at the National Heart, Lung, and Blood Institute, of the National Institutes of Health (NIH). "Additional research on these cells and their products may lead to new ways to diagnose and treat COPD."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Long-term IL-33–producing epithelial progenitor cells in chronic obstructive lung disease

Derek E. Byers, Jennifer Alexander-Brett, Anand C. Patel, Eugene Agapov, Geoffrey Dang-Vu, Xiaohua Jin, Kangyun Wu, Yingjian You, Yael Alevy, Jean-Philippe Girard, Thaddeus S. Stappenbeck, G. Alexander Patterson, Richard A. Pierce, Steven L. Brody, Michael J. Holtzman; J Clin Invest. 2013; doi:10.1172/JCI65570

Washington University School of Medicine

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Instructions for planarian regeneration provided by muscle cells

Main Category: Biology / Biochemistry
Article Date: 20 Aug 2013 - 1:00 PDT Current ratings for:
Instructions for planarian regeneration provided by muscle cells

By studying the planarian flatworm, a master of regenerating missing tissue and repairing wounds, Whitehead Institute Member Peter Reddien and his lab have identified an unexpected source of position instruction: the muscle cells in the planarian body wall.

"I was completely surprised. We had no idea it would be muscle," says Reddien, who is also an associate professor of biology at MIT. "Finding such a cellular system for positional control in an adult regenerative animal was unanticipated and is very informative for understanding regeneration."

For decades, researchers studying regeneration have focused on stem cells, largely because of their ability to spawn almost any type of replacement cell. In fact, the Reddien lab recently determined that cells known as cNeoblasts are the planarian stem cells that are able to regenerate all tissues in these animals.

Long neglected, however, has been the question of cell identity: how do cNeoblasts know where they are and which cells are needed to recreate missing tissues?

The Reddien lab and other labs had already identified various planarian genes involved in imparting positional information during regeneration and adult tissue maintenance, including regulators of Wnt, Bmp, and Fgf signaling pathways. These position control genes (PCGs) are highly conserved and many are found in other animals, including humans. But the cellular location of where those signals originated was unknown.

Reddien hypothesized that a certain type of cell expresses PCGs, possibly a unique type of cell that had not yet been described. To identify these cells, Jessica Witchley and Mirjam Mayer studied PCG expression in planarians and determined that all tested PCGs are indeed expressed in the same cells. They found that collagen, a telltale marker of planarian muscle cells, is also expressed in the same cell population. When part of a planarian was cut off, the muscle cells in the body wall altered which PCGs they expressed in response to the wounding. The lab's results are described in the August 29 issue of Cell Reports.

Until now, the planarian's muscles in the body wall were thought to primarily allow the worms to twist, turn, and respond to touch, in addition to providing some structure to their boneless bodies. Yet, these functions may also explain why muscle cells are so well suited to secrete the proteins coded for by the PCGs.

"Because the muscle cells extend throughout the organism, from head to tail, they are a great way to influence delivery of the PCGs' proteins and get signaling throughout the animal," says Witchley, a co-first author of the Cell Reports paper and a former technician in the Reddien lab. "Because the muscle fibers are long, when you cut the animal, it can immediately respond by contracting to close the wound, turning on wound-induced genes at that site, and eventually changing the pattern of expression to respond to the missing tissue."

The discovery of muscle cells' remarkable role in regeneration opens whole new areas of research.

"For one, we'd like to know how information from muscle cells at the wound site is actually conveyed to the stem cells and how the stem cells receive that information and respond," says Mayer, co-first author and former postdoctoral researcher in the Reddien lab. "And it would be very interesting to see if muscle cells have a position control role in other animals that is similar to what we've found in planarians."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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This work is supported by the National Institutes of Health (NIH grant R01GM080639), the Keck Foundation, and the Helen Hay Whitney Foundation.

Written by Nicole Giese Rura

Peter Reddien's primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a Howard Hughes Medical Institute Investigator and an associate professor of biology at Massachusetts Institute of Technology.

Full Citation:

"Muscle Cells Provide Instructions for Planarian Regeneration"

Cell Reports, 15 August 2013; 10.1016/j.celrep.2013.07.022

Jessica N. Witchley (1,2), Mirjam Mayer (1,2), Daniel E. Wagner (1), Jared H. Owen (1), and Peter W. Reddien (1).

1. Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA

2. These authors contributed equally to this work

Whitehead Institute for Biomedical Research

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Sympathetic neurons engage in "cross talk" with cells in the pancreas during early development

Main Category: Diabetes
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Sympathetic neurons engage in "cross talk" with cells in the pancreas during early development

The human body is a complicated system of blood vessels, nerves, organs, tissue and cells each with a specific job to do. When all are working together, it's a symphony of form and function as each instrument plays its intended roles.

Biologist Rejji Kuruvilla and her fellow researchers uncovered what happens when one instrument is not playing its part.

Kuruvilla along with graduate students Philip Borden and Jessica Houtz, both from the Biology Department at Johns Hopkins University's Krieger School of Arts and Sciences, and Dr. Steven Leach from the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins School of Medicine, recently published a paper in the journal Cell Reports exploring whether "cross-talk" or reciprocal signaling, takes place between the neurons in the sympathetic nervous system and the tissues that the nerves connect to. In this case the targeted tissue called islets, were in the pancreas.

"We knew that sympathetic neurons need molecular signals from the tissues that they connect with, to grow and survive," said Kuruvilla. "What we did not know was whether the neurons would reciprocally signal to the target tissues to instruct them to grow and mature. It made sense to focus on the pancreas because of previous studies done in diabetic animal models where sympathetic nerves within the pancreas were found to retract early on in the disease, suggesting that dysfunction of the nerves could be an early trigger for pancreatic defects."

The researchers spent approximately three years working with lab mice to test the various scenarios in which signaling between sympathetic neurons and islet cells might take place. The experiments focused on what effects removing the sympathetic nerves would have on pancreas development in newborn mice.

Previous studies had shown that pancreatic cells release a signal of their own, a nerve growth protein, that directs the sympathetic nerves toward the pancreas and provides necessary nutrition to sustain the nerves.

In turn, Kuruvilla's team found that in mutant mice, the removal of the sympathetic neurons resulted in deformities in the architecture of the pancreatic islet cells and defects in insulin secretion and glucose metabolism.

Pancreatic islets are highly organized functional micro-organs with a defined size, shape and distinctive arrangement of endocrine cells. It's this marriage of form and function that result in cells clustered close together, that creates greater, more efficient islet cell function.

However, the mutant mice, with their sympathetic neurons removed, had islet formations that were misshapen, sported lesions and developed in a patchy, uneven manner. Because of their dysfunctional islet cell development, postnatal mice did not secrete enough insulin when confronted with high glucose, and had high blood glucose levels as a result. Increased levels of blood glucose in humans is a hallmark of diabetes.

It's known in neuroscience that the neurons in question from the sympathetic nervous system control the body's "flight or fight" response and communicate with connected tissues by releasing a chemical messenger called norepinephrine. The release of norepinephrine also plays an important role in the development and maturation of islets, said Kuruvilla.

Using sympathetic neurons and islet cells grown together in a culture dish, the researchers observed that islet cells move toward the nerves and identified norepinephrine as the nerve signal that causes the movement of the islet cells.

"Seeing how these islet cells were responding to sympathetic neurons both in a dish and the effects of removing the nerves in a whole animal on islet shape and functions were pretty remarkable," said Borden, lead author of the paper. "It was clear to us that sympathetic neurons were key to how islets were developing, something no one else had shown."

Kuruvilla said these studies, identifying sympathetic nerves as a critical player in organizing pancreatic cells during development and influencing their later function, could add to a better understanding of treating diabetes in the future. The research also lends support to the value in considering the importance of external factors such as nerves and blood vessels when transplanting islet cells for the treatment of diabetes in patients.

"This study reveals interactions between two co-developing systems, sympathetic neurons and pancreatic islet cells, that has important implications for peripheral organ development, and for regeneration of these tissues following injury or disease," said Kuruvilla.

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Flavonoids in celery, artichokes kill human pancreatic cancer cells

Main Category: Pancreatic Cancer
Also Included In: Nutrition / Diet
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Flavonoids in celery, artichokes kill human pancreatic cancer cells

Celery, artichokes, and herbs, especially Mexican oregano, all contain apigenin and luteolin, flavonoids that kill human pancreatic cancer cells in the lab by inhibiting an important enzyme, according to two new University of Illinois studies.

"Apigenin alone induced cell death in two aggressive human pancreatic cancer cell lines. But we received the best results when we pre-treated cancer cells with apigenin for 24 hours, then applied the chemotherapeutic drug gemcitabine for 36 hours," said Elvira de Mejia, a U of I professor of food chemistry and food toxicology.

The trick seemed to be using the flavonoids as a pre-treatment instead of applying them and the chemotherapeutic drug simultaneously, said Jodee Johnson, a doctoral student in de Mejia's lab who has since graduated.

"Even though the topic is still controversial, our study indicated that taking antioxidant supplements on the same day as chemotherapeutic drugs may negate the effect of those drugs," she said.

"That happens because flavonoids can act as antioxidants. One of the ways that chemotherapeutic drugs kill cells is based on their pro-oxidant activity, meaning that flavonoids and chemotherapeutic drugs may compete with each other when they're introduced at the same time," she explained.

Pancreatic cancer is a very aggressive cancer, and there are few early symptoms, meaning that the disease is often not found before it has spread. Ultimately the goal is to develop a cure, but prolonging the lives of patients would be a significant development, Johnson added.

It is the fourth leading cause of cancer-related deaths, with a five-year survival rate of only 6 percent, she said.

The scientists found that apigenin inhibited an enzyme called glycogen synthase kinase-3ß (GSK-3ß), which led to a decrease in the production of anti-apoptotic genes in the pancreatic cancer cells. Apoptosis means that the cancer cell self-destructs because its DNA has been damaged.

In one of the cancer cell lines, the percentage of cells undergoing apoptosis went from 8.4 percent in cells that had not been treated with the flavonoid to 43.8 percent in cells that had been treated with a 50-micromolar dose. In this case, no chemotherapy drug had been added.

Treatment with the flavonoid also modified gene expression. "Certain genes associated with pro-inflammatory cytokines were highly upregulated," de Mejia said.

According to Johnson, the scientists' in vitro study in Molecular Nutrition and Food Research is the first to show that apigenin treatment can lead to an increase in interleukin 17s in pancreatic cells, showing its potential relevance in anti-pancreatic cancer activity.

Pancreatic cancer patients would probably not be able to eat enough flavonoid-rich foods to raise blood plasma levels of the flavonoid to an effective level. But scientists could design drugs that would achieve those concentrations, de Mejia said.

And prevention of this frightening disease is another story. "If you eat a lot of fruits and vegetables throughout your life, you'll have chronic exposure to these bioactive flavonoids, which would certainly help to reduce the risk of cancer," she noted.

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Omega-3 rich oils improve membrane fluidity in retina cells and can help fight age-related eye diseases

Main Category: Eye Health / Blindness
Also Included In: Nutrition / Diet;  Seniors / Aging
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Omega-3 rich oils improve membrane fluidity in retina cells and can help fight age-related eye diseases

Scientists working at the Research Center on Aging at the Health and Social Services Centre - University Institute of Geriatrics of Sherbrooke (CSSS-IUGS) have been studying strategies for protecting retinal pigment epithelium (RPE) cells. Dysfunction of the RPE is found in retinopathy and age-related macular degeneration, which is the leading cause of blindness of elderly people in developed countries.

Findings published in the Canadian Journal of Physiology and Pharmacology suggest that incubating retinal cells with vegetable oils induces biochemical and biophysical changes in the cell membrane, which may have a beneficial effect in preventing or slowing the development of retinopathy.

"Membrane fluidity, which refers to the viscosity of the lipid bi-layer of a cell membrane, is a marker of the cell function," explained Prof. A. Khalil, professor at the Université de Sherbrooke and principal investigator of the study. "A decrease of membrane fluidity can affect the rotation and diffusion of proteins and other bio-molecules within the membrane, thereby affecting the functions of these molecules. Whereas, an increase in membrane fluidity makes for a more flexible membrane and facilitates the transmission of light through the eye."

The researchers discovered that vegetable oil fatty acids incorporate in retina cells and increase the plasma membrane fluidity. They concluded that a diet low in trans-unsaturated fats and rich in omega-3 fatty acids and olive oil may reduce the risk of retinopathy. In addition, the research suggests that replacing the neutral oil used in eye drops with oil that possesses valuable biological properties for the eye could also contribute to the prevention of retina diseases.

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The role of stem cells in skin maintenance

Main Category: Dermatology
Also Included In: Stem Cell Research
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
The role of stem cells in skin maintenance

All organs in our body rely on stem cells in order to maintain their function. The skin is our largest organ and forms a shield against the environment. New research results from BRIC, University of Copenhagen and Cambridge University, challenge current stem cell models and explains how the skin is maintained throughout life. The results have just been published in the recognized journal Cell Stem Cell.

New knowledge challenge stem cell models

The skin consists of many different cell types, including hair cells, fat- and sweat glands. It protects us against microbial and chemical attacks and forms a waterproof barrier that prevents fluid loss. Associate professor Kim Jensen' group from BRIC have through mapping of stem cell's behaviour in the skin found out that the skin uses a unique method to renew itself. Their results challenge the current perception of how our skin is renewed.

"Until now, the belief was that the skin's stem cells were organized in a strict hierarchy with a primitive stem cell type at the top of the hierarchy, and that this cell gave rise to all other cell types of the skin. However, our results show that there are differentiated levels of stem cells and that it is their close micro-environment that determines whether they make hair follicles, fat- or sweat glands, says Kim Jensen.

The new research from Kim Jensen completes the stem cell puzzle.

"Our data completes what is already known about the skin and its maintenance. Researchers have until now tried to fit their results into the old model for skin maintenance.

However, the results give much more meaning when we relate them to the new model that our research proposes, says Kim Jensen.

One such example is that it explains the current mystery of how skin cells can divide too much and initiate a skin cancer, without any traces of genetic change in the stem cells believed to maintain the outer layer of the skin. The research from the Jensen group may suggest that the reason that no changes can be found is, that these cells do not take part in the over-proliferation at all.

New knowledge of skin cancer and wound healing

Kim Jensen's research group has used a unique method based on new technology, to understand how the skin is maintained.

"We have marked the early skin stem cell with shining proteins in order to map stem cell behaviour in the outer layer of the skin. The stain is inherited by the daughter cells, so that we can trace their origin and make a family tree. The fine details of the family tree can be used to infer the stem cell's role in normal maintenance of the skin, as well as in wound healing, says Kim Jensen.

An important function of stem cells is to repair damaged tissue. Here, the results from the Jensen groups show that the different stem cell populations collaborate across their normal functions, to repair the skin as fast as possible. However, this can also cause harm, as these changes can "wake up" genes in the stem cells and give rise to cancer. The new results consequently also contribute with new knowledge on the origin of skin cancer.

"Our research will now take two directions. We will establish mathematical models for organ maintenance in order to "measure" what stem cells are doing in the skin. Also, we will expand our investigations in cancer initiation, hoping for results that can contribute to cancer diagnostics and improved treatment, says Kim Jensen.

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The research is supported by a Lundbeck Foundation Fellowship, by the Danish Independent Research Council and the MRC and the Welcome Trust.

The results are published as 'advanced online publication' on August 15th on the journal Cell Stem Cell's homepage, where the printed paper can be found from early October: Page et al - "The Epidermis Comprises Autonomous Compartments Maintained by Distinct Stem Cell Populations." 10.1016/j.stem.2013.07.010

University of Copenhagen

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Where in the body immune cells reach maturity is important for their later function

Main Category: Immune System / Vaccines
Article Date: 16 Aug 2013 - 0:00 PDT Current ratings for:
Where in the body immune cells reach maturity is important for their later function

Regulatory T cells (or "Tregs" for short) play a central role in the human immune system: They guide all of the other immune cells and make sure they are tolerant of the body's own cells and harmless foreign substances. How Tregs become Tregs in the first place has been only incompletely understood - until now. Scientists at the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany, along with their colleagues at the Hannover Medical School (MHH) have recently gleaned important new insights into the workings of these cells. As it turns out, origin is key - greater numbers of Tregs are produced within certain lymph nodes than in others. The researchers are now publishing their insights in the scientific journal Mucosal Immunology.

Without regulatory T cells, the human defence system would not work properly. Defender cells would be fiercely fighting off even harmless foreign substances like the parts of certain kinds of food, for example, as the immune system would simply not be "tolerant" towards these harmless substances. This tolerance is mediated through the Tregs - they are "tolerogenic."

They instruct other immune cells as to which intruders really do need to be fought off and which ones do not pose a threat. However, even regulatory T cells have to first acquire this unique skill. What we have known for some time now is that they receive their "training" inside lymph nodes. "Lymph nodes are basically the immune system's meeting points if you will," says Prof. Jochen Hühn, Head of Experimental Immunology at the HZI. "Here, different types of immune cells meet up and also encounter antigen." An antigen is a structure the immune system is able to recognize like component parts of pathogens or foods.

The researchers compared the development of murine T cells obtained from lymph nodes from various locations in the body, like the liver, intestine, and skin. In the process, they learned that more Tregs capable of teaching other cells to be tolerant of food antigens are made inside lymph nodes of the liver and intestine - a property the lymph nodes maintained even when they were transplanted to the skin. Conversely, skin lymph nodes did not become more tolerogenic if transplanted to the intestine. The HZI scientists made these discoveries together with their colleagues from Prof. Oliver Papst's team at the MHH Institute of Immunology.

Based on their observations, the scientists deduced that lymph node location influences the maturation process of the cells they contain. "The cells retained their original skills for weeks following the transplant," says Dr. Sascha Cording, one of the study's first authors. "You might say lymph nodes have something like a location-specific memory."

And this in spite of the fact that all the various types of blood cells within a lymph node, including the immune cells, are constantly replaced, which means the lymph nodes' location memory must be encoded somewhere in its stroma.

Additional experiments allowed the scientists to probe just how lymph nodes obtain their memory: Following birth, both the supply of vitamin A and the intestinal bacterial microflora figure prominently into this process. Without these two influencing factors, the lymph nodes simply forget about their origin and lose their tolerogenic properties.

These findings about lymph node imprinting apply to humans as well: An inadequate supply of vitamin A after birth or meddling with the baby's developing microflora through administration of antibiotics can interfere with the lymph nodes' long-term memory. "At what age this process happens in humans we cannot as of yet pinpoint with any certainty," says Hühn. "Whether we're talking about the first few days, weeks, or months even, is difficult to surmise." The next step will be identifying the potential repercussions interfering with early imprinting of the immune system. Down the line, things like food allergies or autoimmune diseases might be the result.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject.

The intestinal micro-environment imprints stromal cells to promote efficient Treg induction in gut-draining lymph nodes

Sascha Cording, Benjamin Wahl, Devesha Kulkarni, Himprya Chopra, Jörn Pezoldt, Manuela Buettner, Annegret Dummer, Usri Hadis, Markus Heimesaat, Stefan Bereswill, Christine Falk, Ulrike Bode, Alf Hamann, Diana Fleissner, Jochen Huehn, Oliver Pabst

Mucosal Immunology, 2013, DOI: 10.1038/mi.2013.54

Helmholtz Centre for Infection Research

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Researchers have developed an experimental therapy that can kill human blood cancer cells in the laboratory and eradicate the disease in mice

Main Category: Lymphoma / Leukemia / Myeloma
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
Researchers have developed an experimental therapy that can kill human blood cancer cells in the laboratory and eradicate the disease in mice

Ottawa researchers have developed unique virus-derived particles that can kill human blood cancer cells in the laboratory and eradicate the disease in mice with few side effects. The study is published in Blood Cancer Journal by co-senior authors Drs. David Conrad and John Bell of the Ottawa Hospital Research Institute (OHRI) and the University of Ottawa (uOttawa).

While Dr. Bell and his colleagues have been investigating replicating viruses for the treatment of solid cancers for many years, with very promising results, this is the first major success they have had treating blood cancer (leukemia). It is also the first success they have had using a non-replicating virus-derived particle as opposed to a replicating virus.

"Our research indicated that a replicating virus might not be the safest or most effective approach for treating leukemia, so we decided to investigate whether we could make virus-derived particles that no longer replicate but still kill cancer," said Dr. Conrad, a hematologist conducting research in the Blood and Marrow Transplant Program at The Ottawa Hospital, and currently completing his PhD at OHRI and uOttawa in the Department of Cellular and Molecular Medicine. "We were delighted to see that this novel therapy was very safe at high doses, and worked extremely well in our laboratory leukemia models. We hope to test this in patients in the near future."

The researchers used a specific method and dose of UV light to transform regular replicating viruses into unique particles that could no longer replicate and spread, but could still enter cancer cells efficiently, kill them and stimulate a strong immune response against the cancer. These particles were able to kill multiple forms of leukemia in the laboratory, including samples taken from local patients who had failed all other therapies. Normal blood cells were not affected. This novel treatment was also successful in mouse models of leukemia. In fact, 80 per cent of the mice that received the therapy had markedly prolonged survival and 60 per cent were eventually cured, while all of the untreated mice died of their leukemia within 20 days.

"Leukemia is a devastating disease that can be very difficult to treat, and new therapies are urgently needed," said Dr. Conrad. "While we're still at the early stages of this research, I think this therapy holds a lot of promise because it appears to have a potent, long-lasting effect on leukemia without the debilitating side effects of many cancer therapies used in the clinic right now. We will likely see even better results once we optimize the dose in our preparations to advance this research into human clinical trials."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our lymphoma / leukemia / myeloma section for the latest news on this subject.

This research was funded by the Ontario Institute for Cancer Research, the Terry Fox Foundation, the Natural Sciences and Engineering Research Council of Canada, the Canadian Institutes of Health Research, Ottawa's Department of Medicine and The Ottawa Hospital Foundation.

Non-replicating rhabdovirus-derived particles (NRRPs) eradicate acute leukemia by direct cytolysis and induction of antitumor immunity. Batenchuk C, Le Boeuf F, Stubbert L, Falls T, Atkins HL, Bell JC, and Conrad DP. Blood Cancer J. 2013 Jul 12;3:e123. doi: 10.1038/bcj.2013.23.

Ottawa Hospital Research Institute

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Decellularized mouse heart beats again after regeneration with human heart precursor cells in Pitt project

Main Category: Cardiovascular / Cardiology
Also Included In: Biology / Biochemistry
Article Date: 15 Aug 2013 - 2:00 PDT Current ratings for:
Decellularized mouse heart beats again after regeneration with human heart precursor cells in Pitt project

For the first time, a mouse heart was able to contract and beat again after its own cells were stripped and replaced with human heart precursor cells, said scientists from the University of Pittsburgh School of Medicine. The findings, reported online in Nature Communications, show the promise that regenerating a functional organ by placing human induced pluripotent stem (iPS) cells - which could be personalized for the recipient - in a three-dimensional scaffold could have for transplantation, drug testing models and understanding heart development.

In the United States, one person dies of heart disease every 34 seconds, and more than 5 million people suffer from heart failure, meaning a reduced ability to pump blood, said senior investigator Lei Yang, Ph.D., assistant professor of developmental biology, Pitt School of Medicine. More than half of heart disease patients do not respond to current therapies and there is a scarcity of donor organs for transplant.

"Scientists have been looking to regenerative medicine and tissue engineering approaches to find new solutions for this important problem," Dr. Yang said. "The ability to replace a piece of tissue damaged by a heart attack, or perhaps an entire organ, could be very helpful for these patients."

For the project, the research team first "decellularized," or removed all the cells, from a mouse heart, a process that takes about 10 hours using a variety of agents. Then, they repopulated the remaining heart framework, or scaffold, with multipotential cardiovascular progenitor (MCP) cells. These replacement cells were produced by reverse engineering fibroblast cells from a small skin biopsy to make induced pluripotent stem cells and then treating the iPS cells with special growth factors to further induce differentiation.

"This process makes MCPs, which are precursor cells that can further differentiate into three kinds of cells the heart uses, including cardiomyocytes, endothelial cells and smooth muscle cells," Dr. Yang explained. "Nobody has tried using these MCPs for heart regeneration before. It turns out that the heart's extracellular matrix - the material that is the substrate of heart scaffold - can send signals to guide the MCPs into becoming the specialized cells that are needed for proper heart function."

After a few weeks, the mouse heart had not only been rebuilt with human cells, it also began contracting again, at the rate of 40 to 50 beats per minute, the researchers found. More work must be done to make the heart contract strongly enough to be able to pump blood effectively, and to rebuild the heart's electrical conduction system correctly so that the heart rate speeds up and slows down appropriately.

In the future, it might be possible to take a simple skin biopsy from a patient to derive personalized MCPs that can be used to seed a biologic scaffold and regenerate a replacement organ suitable for transplantation, Dr. Yang noted. The model also could be used as a lab-based method to preclinically test the effect of new drugs on the heart or to study how the fetal heart might develop.

"One of our next goals is to see if it's feasible to make a patch of human heart muscle," he added. "We could use patches to replace a region damaged by a heart attack. That might be easier to achieve because it won't require as many cells as a whole human-sized organ would."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cardiovascular / cardiology section for the latest news on this subject.

The project was funded by the University of Pittsburgh, the American Heart Association, and the National Science Council (Taiwan).

Repopulation of decellularized mouse heart with human induced pluripotent stem cell-derived cardiovascular progenitor cells

Nature Communications 4, Article number: 2307 doi:10.1038/ncomms3307

Tung-Ying Lu, Bo Lin, Jong Kim, Mara Sullivan, Kimimasa Tobita, Guy Salama & Lei Yang

University of Pittsburgh

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Mice experience therapeutic changes in glioma after transplantation of neural stem cells

Main Category: Neurology / Neuroscience
Also Included In: Cancer / Oncology;  Stem Cell Research
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
Mice experience therapeutic changes in glioma after transplantation of neural stem cells

Neural stem cells transplanted into tumor-bearing rats can hinder tumor cell growth and proliferation; however, the mechanism remains unclear.

Abnormal activation of the Ras/Raf/Mek/Erk signaling cascade plays an important role in glioma.

Inhibition of this aberrant activity could effectively hinder glioma cell proliferation and promote cell apoptosis.

To investigate the mechanism of glioblastoma treatment by neural stem cell trans-plantation with respect to the Ras/Raf/Mek/Erk pathway, Hua Li and team from the 476 Hospital of Chinese PLA observed Raf-1, Erk and Bcl-2 protein expression as well as Caspase-3 protein expression.

The researchers found that transplantation of neural stem cells could inhibit the abnormal activation of Ras/Raf/Mek/Erk signaling, thus promoting apoptosis and potentially treating glioma.

These findings are published in Neural Regeneration Research (Vol. 8, No. 19, 2013).

Article: " Apoptosis in glioma-bearing rats after neural stem cell transplantation " by Hua Li1, Zhenjun Chen1, Shaopeng Zhou2 (1 Department of Neurology, the 476 Hospital of Chinese PLA, Fuzhou 350002, Fujian Province, China; 2 Department of Anesthesiology, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, Guangdong Province, China)

Li H, Chen ZJ, Zhou SP. Apoptosis in glioma-bearing rats after neural stem cell transplantation. Neural Regen Res. 2013;8(19):1793-1802. doi:10.3969/j.issn.1673-5374.2013.19.007

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Characterizing stem cells in larval schistosomes may help control the prolific human parasite

Main Category: Infectious Diseases / Bacteria / Viruses
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
Characterizing stem cells in larval schistosomes may help control the prolific human parasite

Ancient Egyptian mummies revealed that humans have been hosting parasitic flatworms called schistosomes for more than 5,000 years. Today the parasites continue to plague millions of people across the world, causing roughly 250,000 deaths each year.

The schistosome reproductive cycle results in exponentially more schistosomes each generation. Not only do the adults lay hundreds to thousands of eggs each day but the larval schistosomes are able to clone themselves thousands of times, with each clone capable of developing into an egg-producing adult.

Researchers at the University of Illinois quickly realized that one key to controlling schistosomes is being able to control their incredibly prolific life cycle. In a recent study published in the journal eLife, Illinois researchers have come one step closer to understanding the unique mechanisms that allow schistosomes' germinal cells, stem cells that multiply into other types of cells, to create thousands of clonal larvae that can then infect humans.

The Disease

This work adds to our understanding of the basic biology of schistosomiasis, a chronic disease caused by schistosome parasites, that robbed at least 243 million people of their productivity in 2011.

"People don't feel well, and so they are not productive in their work," said James Collins III, a postdoctoral researcher in the Department of Cell and Developmental Biology (CDB) at Illinois. "This disease keeps them from being able to realize their full potential, and in turn, they remain poor and are exposed to more diseases like schistosomiasis, which are ultimately diseases of sanitation. It's a disease of poverty that also perpetuates poverty."

Schistosomiasis can result in abdominal pain, diarrhea, and blood in urine or feces. The parasite's eggs, and not the parasite itself, cause these symptoms and others. The bloodstream carries many of the eggs to the liver and other areas of the body where they can trigger a massive immune response.

"When you look at people who have a high level of infection, you see many holes in their liver," said Phillip Newmark, a Professor of Cell and Developmental Biology at Illinois, an Investigator of the Howard Hughes Medical Institute, and an affiliate of the Regenerative Biology and Tissue Engineering research theme at the Institute for Genomic Biology (IGB). "Where there was an egg, a hole is formed where the tissue has been destroyed by the host immune system's inflammatory response."

The Life Cycle

Every day for decades, adult schistosomes can lay hundreds to thousands of eggs. Their life cycle starts over when the eggs are excreted from the human host through urine or feces. When the eggs contact water, they hatch out "miracidia" that seek out the snail intermediate hosts.

Inside the correct species of snail, the miracidia become sporocysts, essentially sacs filled with germinal cells, that undergo clonal expansion, making tens to hundreds of thousands of copies of themselves in the form of "cercariae." The fast-swimming cercariae are shed from the snail, and search for human hosts who find themselves in cercariae-infested fresh water.

"They are attracted by the fatty acids in your skin," said Collins. "In the lab, you can leave your thumbprint on a plastic petri dish, and all the cercariae will swarm to your thumbprint and try to penetrate the plastic."

Once they find a host, they are able to burrow through the skin and enter the bloodstream. Inside the body, they migrate to specific sites in the human host, mature into male or female worms, and find mates with whom they will live, paired together "in copula." If left undetected, they will continue mass producing eggs for decades.

The Research

Illinois researchers are approaching this important problem from a unique perspective, using developmental biology (the study of how organisms grow and develop) and applying the lessons they have learned from studying planarians, non-parasitic relatives of schistosomes.

"When researchers are just focused on targeting diseases and developing drugs, they may wind up limiting their opportunities by not really understanding the biology of the system," Newmark said. "I think fundamental, curiosity-driven research is still vital for developing long-lasting solutions. If anything comes of this, it will be because we were asking very fundamental questions about these parasites, based upon our knowledge of their free-living cousins, the planarians."

The team's research was motivated by the idea that stem cells seem to be key to schistosomes' ability to live within humans, but also to their ability to live and clone themselves within their snail hosts.

They discovered that germinal cells possess a molecular signature - a collection of expressed genes - that is similar to that of neoblasts (adult stem cells) that allow planarians to regrow missing body parts. Among these genes, they identified some that are required for maintaining the germinal cell population.

This evidence suggests that schistosome larvae may have evolved by adapting a developmental program used by non-parasitic flatworms in order to rapidly increase their population - essentially giving them the opportunity to reproduce twice within their life cycle, once asexually inside snail hosts and once sexually inside human hosts.

Illinois researchers believe they can apply this newfound developmental knowledge to future studies that may lead to ways to control, or even eradicate, schistosomes. They have already discovered that they can make the reproductive system of a planarian disappear by removing the function of a neuropeptide; eventually, they hope to do the same in schistosomes.

Still, there's much to still be learned, says Collins. "We have really only scratched the surface of understanding the basic biology of these organisms. In order to be able to treat this disease, we need to know more about the organisms that cause it. That's one of our main motivations for this work."

First author Bo Wang, a postdoctoral fellow at the IGB, said the obvious next step will be to further characterize these schistosome cells on a genomic level. "We really need to improve our understanding of schistosome stem cells," Wang said. "We still don't understand all the mechanisms that really make them unique, that really make them have this tremendous capacity to proliferate, or reproduce."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

The National Institutes of Allergy and Infectious Diseases (NIAID) funded this study. Wang was also supported by the IGB, who sponsored his fellowship. The work was reported in the July 30, 2013 issue of eLife (doi.org/10.7554/eLife.00768).

Institute for Genomic Biology, University of Illinois at Urbana-Champaign

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Potential use of Excellagen to repair prenatally diagnosed birth defects using mesenchymal stem cells

Main Category: Stem Cell Research
Article Date: 14 Aug 2013 - 2:00 PDT Current ratings for:
Potential use of Excellagen to repair prenatally diagnosed birth defects using mesenchymal stem cells

Cardium Therapeutics has reported on a research collaboration with researchers at Boston Children's Hospital, to assess the medical utility of Excellagen® as a delivery scaffold to seed autologous mesenchymal fetal stem cells for ex-vivo engineering of tissue grafts for transplantation into infants to repair prenatally diagnosed birth defects.

Autologous mesenchymal fetal stem cells are derived prenatally from infants with a medical defect requiring life-saving tissue repairs. These stem cells are sourced from amniotic fluid, the placenta or umbilical cord blood. The stem cells are then seeded into a scaffold to promote the growth of an engineered tissue graft. These grafts will potentially be used to surgically repair, either in the fetus or immediately following birth, certain prenatally diagnosed birth defects that could include congenital diaphragmatic hernia, tracheal and chest wall defects, bladder extrophy and various cardiac anomalies. Preliminary pre-clinical research has confirmed that Excellagen collagen homogenate maintains mesenchymal fetal stem cell viability. Additional proof of concept studies are currently underway.

"Boston Children's team has made remarkable progress in the field of tissue regeneration and surgical repair of prenatally diagnosed congenital defects. We believe that Excellagen has an opportunity serve as a delivery platform in the field of stem cell therapy and we look forward to continuing to work with the Boston Children's team to help make their innovative therapeutic vision a new standard of care, and potentially advance stem cell therapies toward commercialization," stated Christopher J. Reinhard, Chairman and Chief Executive Officer of Cardium. "Excellagen was specifically designed to support advanced biologics and this new application further highlights its potential versatility as an important delivery agent for a variety of innovative therapeutic applications."

Cardium's FDA-cleared Excellagen is an aseptically-manufactured, quaternary fibrillar Type I bovine collagen homogenate that is configured into a staggered array of three-dimensional, triple helical, telopeptide-deleted, tropocollagen molecules. This linear array forms a flowable, biocompatible and bioactive structural matrix that can promote chemotaxis, cellular adhesion, migration and proliferation to stimulate tissue formation. The Excellagen homogenate represents a new product delivery platform that allows for the potential development of a portfolio of advanced tissue regeneration therapeutic opportunities that could include anti-infectives, antibiotics, peptides, proteins, small molecules, DNA, stem cells, differentiated cells and conditioned cell media.

Excellagen is a syringe-based, professional-use, pharmaceutically-formulated 2.6% fibrillar Type I bovine collagen homogenate that functions as an acellular biological modulator to activate the wound healing process and significantly accelerate the growth of granulation tissue. Excellagen's FDA clearance provides for very broad labeling including partial and full-thickness wounds, pressure ulcers, venous ulcers, diabetic ulcers, chronic vascular ulcers, tunneled/undermined wounds, surgical wounds (donor sites/graft, post-Mohs surgery, post-laser surgery, podiatric, wound dehiscence), trauma wounds (abrasions, lacerations, second-degree burns and skin tears) and draining wounds. Excellagen is intended for professional use following standard debridement procedures in the presence of blood cells and platelets, which are involved with the release of endogenous growth factors. Excellagen's unique fibrillar Type I bovine collagen homogenate formulation is topically applied through easy-to-control, pre-filled, sterile, single-use syringes and is designed for application at only one-week intervals.

There have been important, positive findings reported by physicians using Excellagen as part of Cardium's physician sampling, patient outreach and market "seeding" programs. In several case studies, physicians reported a rapid onset of the growth of granulation tissue in a wide array of wounds, including non-healing diabetic foot ulcers (consistent with the results of Cardium's Matrix clinical study), as well as pressure ulcers, venous ulcers and Mohs surgical wounds. In certain cases, rapid granulation tissue growth and wound closure have been achieved with Excellagen following unsuccessful treatment with other advanced wound care approaches. From a dermatology perspective, a previously unexplored vertical market, remarkable healing responses have been observed following Mohs surgery for patients diagnosed with squamous and basal cell carcinomas, including deep surgical wounds extending to the periosteum (a membrane that lines the outer surface of bones). Additionally, because of the easy-use and platelet activating capacity, physicians have been employing Excellagen in severe non-healing wounds at near-amputation status, in combination with autologous platelet-rich plasma therapy and collagen sheet products. These case studies and positive physician feedback provide additional support of Excellagen's potential utility as an important new tool to help promote the wound healing process. Excellagen case studies are available at http://www.excellagen.com/surgical-wounds.html.

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Research suggests neural stem cells may regenerate after anti-cancer treatment

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience;  Radiology / Nuclear Medicine
Article Date: 14 Aug 2013 - 1:00 PDT Current ratings for:
Research suggests neural stem cells may regenerate after anti-cancer treatment

Scientists have long believed that healthy brain cells, once damaged by radiation designed to kill brain tumors, cannot regenerate. But new Johns Hopkins research in mice suggests that neural stem cells, the body's source of new brain cells, are resistant to radiation, and can be roused from a hibernation-like state to reproduce and generate new cells able to migrate, replace injured cells and potentially restore lost function.

"Despite being hit hard by radiation, it turns out that neural stem cells are like the special forces, on standby waiting to be activated," says Alfredo Quiñones-Hinojosa, M.D., a professor of neurosurgery at the Johns Hopkins University School of Medicine and leader of a study described online in the journal Stem Cells. "Now we might figure out how to unleash the potential of these stem cells to repair human brain damage."

The findings, Quiñones-Hinojosa adds, may have implications not only for brain cancer patients, but also for people with progressive neurological diseases such as multiple sclerosis (MS) and Parkinson's disease (PD), in which cognitive functions worsen as the brain suffers permanent damage over time.

In Quiñones-Hinojosa's laboratory, the researchers examined the impact of radiation on mouse neural stem cells by testing the rodents' responses to a subsequent brain injury. To do the experiment, the researchers used a device invented and used only at Johns Hopkins that accurately simulates localized radiation used in human cancer therapy. Other techniques, the researchers say, use too much radiation to precisely mimic the clinical experience of brain cancer patients.

In the weeks after radiation, the researchers injected the mice with lysolecithin, a substance that caused brain damage by inducing a demyelinating brain lesion, much like that present in MS. They found that neural stem cells within the irradiated subventricular zone of the brain generated new cells, which rushed to the damaged site to rescue newly injured cells. A month later, the new cells had incorporated into the demyelinated area where new myelin, the protein insulation that protects nerves, was being produced.

"These mice have brain damage, but that doesn't mean it's irreparable," Quiñones-Hinojosa says. "This research is like detective work. We're putting a lot of different clues together. This is another tiny piece of the puzzle. The brain has some innate capabilities to regenerate and we hope there is a way to take advantage of them. If we can let loose this potential in humans, we may be able to help them recover from radiation therapy, strokes, brain trauma, you name it."

His findings may not be all good news, however. Neural stem cells have been linked to brain tumor development, Quiñones-Hinojosa cautions. The radiation resistance his experiments uncovered, he says, could explain why glioblastoma, the deadliest and most aggressive form of brain cancer, is so hard to treat with radiation.

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The research was supported by grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (RO1 NS070024), the Maryland Stem Cell Research Fund, the Robert Wood Johnson Foundation, the Howard Hughes Medical Institute, the PROMETEO grant, the Red de Terapia Celular (TerCel) from Instituto de Salud Carlos III, and the Consejo Nacional de Ciencia y Tecnología.

Other Johns Hopkins researchers involved in the study include Vivian Capilla-Gonzalez, Ph.D.; Hugo Guerrero-Cazares, M.D., Ph.D.; Janice Bonsu; Oscar Gonzalez-Perez, M.D.; Pragathi Achanta, Ph.D.; John Wong, Ph.D.; and Jose Manuel Garcia-Verdugo, Ph.D.

Johns Hopkins Medicine

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'Research suggests neural stem cells may regenerate after anti-cancer treatment'

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Stem cells in urine easy to isolate and have potential for numerous therapies

Main Category: Stem Cell Research
Article Date: 03 Aug 2013 - 0:00 PDT Current ratings for:
Stem cells in urine easy to isolate and have potential for numerous therapies

Could harvesting stem cells for therapy one day be as simple as asking patients for a urine sample? Researchers at Wake Forest Baptist Medical Center's Institute for Regenerative Medicine and colleagues have identified stem cells in urine that can be directed to become multiple cell types.

"These cells can be obtained through a simple, non-invasive low-cost approach that avoids surgical procedures," said Yuanyuan Zhang, M.D., Ph.D., assistant professor of regenerative medicine and senior researcher on the project.

Reporting online in the journal Stem Cells, the team successfully directed stem cells from urine to become bladder-type cells, such as smooth muscle and urothelial, the cells that line the bladder. But the urine-derived cells could also form bone, cartilage, fat, skeletal muscle, nerve, and endothelial cells, which line blood vessels. The multipotency of the cells suggests their use in a variety of therapies.

"These stem cells represent virtually a limitless supply of autologous cells for treating not only urology-related conditions such as kidney disease, urinary incontinence and erectile dysfunction, but could be used in other fields as well," said Zhang. "They could also potentially be used to engineer replacement bladders, urine tubes and other urologic organs."

Being able to use a patient's own stem cells for therapy is considered advantageous because they do not induce immune responses or rejection. However, because tissue-specific cells are a very small subpopulation of cells, they can be difficult to isolate from organs and tissues.

Zhang's team first identified the cells, which are a small subset of the many cells found in urine, in 2006. The current research builds on earlier studies by confirming the multipotency of the cells. In addition, the research found that unlike iPS cells or embryonic stem cells, the urine derived-stem cells do not form tumors when implanted in the body, indicating they may be safe for use in patients.

The research involved obtaining urine samples from 17 healthy individuals ranging in age from five to 75 years. Isolating the cells from urine involves minimal processing, according to the authors. Next, they evaluated the cells' ability to become multiple cell types.

Importantly, the cells differentiated into the three tissue layers (endoderm, ectoderm and mesoderm) that are a hallmark of true stem cells and also differentiated into the specific cell types mentioned earlier.

Next, the researchers placed cells that had been differentiated into smooth muscle and urothelial cells onto scaffolds made of pig intestine. When implanted in mice for one month, the cells formed multi-layer, tissue-like structures.

The urine-derived stem cells have markers of mesenchymal cells, which are adult stem cells from connective tissue such as bone marrow. They also have markers for pericytes, a subset of mesenchymal cells found in small blood vessels.

Where do the cells come from? Researchers suspect that the cells originate from the upper urinary tract, including the kidney. Female study participants who had received kidney transplants from male donors were found to have the y chromosome in their urine-derived stem cells, suggesting the kidney as the source of the cells.

"Identifying the origins of the cells will lead to a better understanding of the biology of this multipotent population of mesenchymal cells within the urinary tract system," said Zhang.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Co-researchers were Shantaram Bharadwaj, Ph.D., Guihua Liu, M.D., Ph.D., Yingai Shi, M.D., Ph.D., Rongpei Wu, M.D., Ph.D., Bin Yang, M.D., Ph.D., Anthony Atala, M.D., and Jan Rohozinski, Ph.D ., Wake Forest Baptist; Tong-chan He, M.D., Ph.D., the University of Chicago Medical Center; Yuxin Fan, M.D., Ph.D., and Xinyan Lu, M.D., Baylor College of Medicine; Xiaobo Zhou, Ph.D., the Methodist Hospital Research Institute; and Hong Liu, Ph.D., University of Oklahoma.

Wake Forest Baptist Medical Center

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The flexible tail of the prion protein poisons brain cells

Main Category: CJD / vCJD / Mad Cow Disease
Also Included In: Neurology / Neuroscience;  Biology / Biochemistry
Article Date: 03 Aug 2013 - 0:00 PDT Current ratings for:
The flexible tail of the prion protein poisons brain cells

Prion proteins are the infectious pathogens that cause Mad Cow Disease and Creutzfeldt-Jakob disease. They occur when a normal prion protein becomes deformed and clumped. The naturally occurring prion protein is harmless and can be found in most organisms. In humans, it is found in our brain cell membrane. By contrast, the abnormally deformed prion protein is poisonous for the brain cells. Adriano Aguzzi, Professor of Neuropathology at the University of Zurich and University Hospital Zurich, has spent many years exploring why this deformation is poisonous. Aguzzi's team has now discovered that the prion protein has a kind of «switch» that controls its toxicity. This switch covers a tiny area on the surface of the protein. If another molecule, for example an antibody, touches this switch, a lethal mechanism is triggered that can lead to very fast cell death.

Flexible tail induces cell death

In the current edition of «Nature», the scientists demonstrate that the prion protein molecule comprises two functionally distinct parts: a globular domain, which is tethered to the cell membrane, and a long and unstructured tail. Under normal conditions, this tail is very important in order to maintain the functioning of nerve cells. By contrast, in the case of a prion infection the pathogenic prion protein interacts with the globular part and the tail causes cell death - this is the hypothesis put forward by the researchers.

Aguzzi and his team tested this by generating mimetic antibodies in tissue sections from the cerebellum of mice which have a similar toxicity to that of a prion infection. The researchers found that these antibodies tripped the switch of the prion protein. «Prion proteins with a trimmed version of the flexible tail can, however, no longer damage the brain cells, even if their switch has been recognized by antibodies», explains Adriano Aguzzi. "This flexible tail is responsible for causing cell death." If the tail is bound and made inaccessible using a further antibody, activation of the switch can likewise no longer trigger cell death.

"Our discovery has far-reaching consequences for understanding prion diseases", says Aguzzi. The findings reveal that only those antibodies that target the prion protein tail are suitable for use as potential drugs. By contrast, antibodies that trip the switch of the prion are very harmful and dangerous.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Tracking nanodiamond-tagged stem cells

Main Category: Stem Cell Research
Article Date: 04 Aug 2013 - 10:00 PDT Current ratings for:
Tracking nanodiamond-tagged stem cells

A method that is used to track the fate of a single stem cell within mouse lung tissue is reported in a study published online this week in Nature Nanotechnology. The method may offer insights into the factors that determine the acceptance of transplanted stem cells, and their ability to regenerate within a host.

Stem cell therapy has the potential to repair and regenerate damaged tissues. Implanted cells might, however, be rejected, migrate or die; tracking stem cells in vivo may help to further understand what happens once these cells are inside the host.

Huan-Cheng Chang and colleagues used fluorescent nanodiamonds to tag lung stem cells and implant them in mice with damaged lungs. They found that not only did the damaged lung cells of the mice restore rapidly, but that the uptake and regeneration of stem cells could be tracked with single-cell resolution.

The authors suggest that, in the future, the technique could also be used to monitor the uptake of different kinds of stem cell, such as bone marrow stem cells.

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Tracking nanodiamond-tagged stem cells

Nature Nanotechnology - DOI: 10.1038/nnano.2013.147

Nature

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Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

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Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

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