Category Archives: Stem Cells

Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) have developed a novel technique to promote tissue repair in damaged muscles. The technique also creates a sustainable pool of muscle stem cells needed to support multiple rounds of muscle repair. The study, published September 7 in Nature Medicine, provides promise for a new therapeutic approach to treating the millions of people suffering from muscle diseases, including those with muscular dystrophies and muscle wasting associated with cancer and aging.

There are two important processes that need to happen to maintain skeletal-muscle health. First, when muscle is damaged by injury or degenerative disease such as muscular dystrophy, muscle stem cells -- or satellite cells -- need to differentiate into mature muscle cells to repair injured muscles. Second, the pool of satellite cells needs to be replenished so there is a supply to repair muscle in case of future injuries. In the case of muscular dystrophy, the chronic cycles of muscle regeneration and degeneration that involve satellite-cell activation exhaust the muscle stem-cell pool to the point of no return.

"Our study found that by introducing an inhibitor of the STAT3 protein in repeated cycles, we could alternately replenish the pool of satellite cells and promote their differentiation into muscle fibers," said Alessandra Sacco, Ph.D., assistant professor in the Development, Aging, and Regeneration Program at Sanford-Burnham. "Our results are important because the process works in mice and in human muscle cells."

"Our next step is to see how long we can extend the cycling pattern, and test some of the STAT3 inhibitors currently in clinical trials for other indications such as cancer, as this could accelerate testing in humans," added Sacco.

"These findings are very encouraging. Currently, there is no cure to stop or reverse any form of muscle-wasting disorders -- only medication and therapy that can slow the process," said Vittorio Sartorelli, M.D., chief of the Laboratory of Muscle Stem Cells and Gene Regulation and deputy scientific director at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). "A treatment approach consisting of cyclic bursts of STAT3 inhibitors could potentially restore muscle mass and function in patients, and this would be a very significant breakthrough."

Revealing the mechanism of STAT3

STAT3 (signal transducer and activator of transcription 3) is a protein that activates the transcription of genes in response to IL-6, a signaling protein released by cells in response to injury and inflammation. Prior to the study, scientists knew that STAT3 played a complex role in skeletal muscle, promoting tissue repair in some instances and hindering it in others. But the precise mechanism of how STAT3 worked was a mystery.

The research team first used normally aged mice and mice models of a form of muscular dystrophy that resembles the human disease to see what would happen if they were given a drug to inhibit STAT3. They found that the inhibitor initially promoted satellite-cell replication, followed by differentiation of the satellite cells into muscle fibers. When they injected the STAT3 inhibitor every seven days for 28 days, they found an overall improvement in skeletal-muscle repair, and an increase in the size of muscle fibers.

"We were pleased to find that we achieved similar results when we performed the experiments in human muscle cells," said Sacco. "We have discovered that by timing the inhibition of STAT3 -- like an "on/off" light switch -- we can transiently expand the satellite-cell population followed by their differentiation into mature muscle cells."

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Researchers discover key to making new muscles

As we age, stem cells throughout our bodies gradually lose their capacity to repair damage, even from normal wear and tear. Researchers from the Ottawa Hospital Research Institute and University of Ottawa have discovered the reason why this decline occurs in our skeletal muscle. Their findings were published online in the influential journal Nature Medicine.

A team led by Dr. Michael Rudnicki, senior scientist at the Ottawa Hospital Research Institute and professor of medicine at the University of Ottawa, found that as muscle stem cells age, their reduced function is a result of a progressive increase in the activation of a specific signalling pathway. Such pathways transmit information to a cell from the surrounding tissue. The particular culprit identified by Dr. Rudnicki and his team is called the JAK/STAT signalling pathway.

"What's really exciting to our team is that when we used specific drugs to inhibit the JAK/STAT pathway, the muscle stem cells in old animals behaved the same as those found in young animals," said Dr. Michael Rudnicki, a world leader in muscle stem cell research. "These inhibitors increased the older animals' ability to repair injured muscle and to build new tissue."

What's happening is that our skeletal muscle stem cells are not being instructed to maintain their population. As we get older, the activity of the JAK/STAT pathway shoots up and this changes how muscle stem cells divide. To maintain a population of these stem cells, which are called satellite cells, some have to stay as stem cells when they divide. With increased activity of the JAK/STAT pathway, fewer divide to produce two satellite cells (symmetric division) and more commit to cells that eventually become muscle fibre. This reduces the population of these regenerating satellite cells, which results in a reduced capacity to repair and rebuild muscle tissue.

While this discovery is still at early stages, Dr. Rudnicki's team is exploring the therapeutic possibilities of drugs to treat muscle-wasting diseases such as muscular dystrophy. The drugs used in this study are commonly used for chemotherapy, so Dr. Rudnicki is now looking for less toxic molecules that would have the same effect.

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The above story is based on materials provided by Ottawa Hospital Research Institute. Note: Materials may be edited for content and length.

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Why age reduces stem cells' ability to repair muscle

Durham, NC (PRWEB) September 05, 2014

A study published in STEM CELLS on August 30, 2014, details a new, simple, and highly efficient way to convert cells taken from an adults skin into stem cells that have the potential to differentiate into white blood cells.

Stem cells are the keystone of regenerative medicine due to their ability to be coaxed into becoming nearly any cell in the body. Induced pluripotent stem cells (iPSCs) are of particular interest because they can be generated directly from adult cells and thus many of the controversies associated with embryonic stem cells are avoided.

However, a major problem with iPSCs is their propensity to differentiate into immature cells. This is particularly true of hematopoietic (blood) cells, and the ability to generate long-term, re-populating hematopoietic stem cells has long eluded researchers.

In terms of potential clinical applications, the hematopoietic system represents one of the most suitable tissues for stem cell-based therapies as it can be relatively easily reconstituted upon bone marrow or umbilical cord blood cell transplantation. However, and even though much effort has focused on the derivation of hematopoietic cells from iPSCs, their grafting and differentiation potential remains limited, said Juan Carlos Izpisua Belmonte, Ph.D., of the Salk Institute for Biological Studies, La Jolla, Calif.

He and his colleagues at the Salk Institute, the Center of Regenerative Medicine in Barcelona, and the Centre for Biomedical Network Research on Rare Diseases (CIBERER), Madrid, decided to tackle this problem using a gene called Sox2 and a gene-regulating molecule called miRNA 125b. The Sox2 gene was used as a primer to coax human fibroblasts (the most common cells of connective tissue in animals) into differentiating into CD34+ cells, which are primitive blood- and bone marrow-derived progenitor cells. The miRNA 125b was then added to facilitate the differentiation of these CD34+ stem cells into more mature, hematopoietic-like stem cells.

To our knowledge this is the first time human skin cells have been converted into white blood-like cells with reconstitution and migratory potential, able to further mature in vivo and, more importantly, to graft into distant hematopoietic sites Dr. Belmonte said. Our results indicate this strategy could help circumvent obstacles to reprogramming human cells into blood cells that have clinical potential.

Jan Nolta,Ph.D., Editor-in-Chief of STEM CELLS, said, we are proud to feature this interesting work that shows that miRNA 125b facilitates the differentiation of fibroblast-derived progenitors into more mature, hematopoietic-like stem cells. This is exciting for future research into the blood-forming system. ###

The full article, Conversion of Human Fibroblasts into Monocyte-Like Progenitor Cells, can be accessed at http://onlinelibrary.wiley.com/doi/10.1002/stem.1800/abstract.

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New Study Shows Simple Conversion of Skin Cells Into White Blood-Like Cells

ALS ice bucket challenge - Carlsbad Stem Cells R D
Thermo Fisher Scientific Transfection team challenged us and here we are. Keeping in mind the severe drought in California, we used ice used in the lab and carried out the challenge by a water...

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Carol Marchetto, Ph.D. - "Using human pluripotent stem cells to model autism spectrum disorders
Carol Marchetto is a Senior Staff Scientist in the Laboratory of Dr. Fred Gage at The Salk Institute. Carol is involved in understanding the mechanisms by which human pluripotent stem cells...

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LEXXTEX 008 - THE SECRET REVEALED " STEM CELLS VS GENES "
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Human trials on the effectiveness of using adult stem cells in the fight against cornea transplant rejection could be under way within the next five years.

Corneal eye disease is the fourth most common cause of blindness in the world and affects more than 10 million people worldwide. New research from NUI Galway has found that transplant rejection rates could be reduced to as low as 10% by administering a stem cell grown from the bone marrow of adult donors.

Although 100,000 people worldwide undergo cornea transplants each year, about 30% are unsuccessful due to rejection by the patients own immune system.

An unhealthy cornea affects vision by scattering or distorting light and causing glare and blurred vision.

Corneal transplants are the most widely used treatments where the diseased or scarred cornea is replaced with healthy tissue from an organ donor.

Researchers from NUI Galways Regenerative Medicine Institute previously found that mesenchymal stem cells (MSC) release chemicals capable of adjusting the immune system balance in the body.

The cells can be readily obtained and grown from the bone marrow of adult donors and the finding led them to study their usefulness in combating cornea transplant rejection.

The teams lead scientist, Dr Oliver Treacy, said the model system they developed led to an increase in cells called regulatory T-cells, which dampen down inflammation, and a decrease in the number of natural killer cells, key players in the rejection process.

Consultant ophthalmologist at Galway University Hospital, Gerry Fahy, who was involved in the study, said corneal transplant rejection could result in blindness and was not uncommon in high-risk patients.

This important research presents a potentially new avenue of treatment to prevent transplant rejection and save vision in this vulnerable group of patients, said Mr Fahy.

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Stem cells could cut high rate of cornea transplant rejection

Stem Cells - LUB DUB #39;s second issue scientific teaser!
A little bit of what you #39;re expecting with the scientific section of our second issue! Don #39;t forget to visit our booth this October! LIKE and FOLLOW us here ...

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Newswise DALLAS Sept. 4, 2014 Rare stem cells in testis that produce a biomarker protein called PAX7 help give rise to new sperm cells and may hold a key to restoring fertility, research by scientists at UT Southwestern Medical Center suggests.

Researchers studying infertility in mouse models found that, unlike similar types of cells that develop into sperm, the stem cells that express PAX7 can survive treatment with toxic drugs and radiation. If the findings hold true in people, they eventually could lead to new strategies to restore or protect fertility in men undergoing cancer treatment.

Unfortunately, many cancer treatments negatively impact fertility, and men who receive such treatments are at high risk of losing their fertility. This is of great concern among cancer patients, said Dr. Diego H. Castrillon, Associate Professor of Pathology and Director of Investigative Pathology. The PAX7 stem cells we identified proved highly resistant to cancer treatments, suggesting that they may be the cells responsible for the recovery of fertility following such treatments.

Infertility, which the Centers for Disease Control estimates affects as many as 4.7 million men in the United States, is a key complication of cancer treatments, such as chemotherapy and radiation therapy.

The new findings, presented in the Journal of Clinical Investigation, provide valuable insight into the process of sperm development. Known as spermatogenesis, sperm development is driven by a population of immature stem cells called progenitors in the testes. These cells gradually mature into fully differentiated sperm cells. Dr. Castrillon and his team tracked progenitor cells that express the protein PAX7 in mouse testes, and found that these cells gradually give rise to mature sperm.

We have long known that male fertility is driven by rare stem cells within the testes, but the precise identity of these stem cells has been disputed, said Dr. Castrillon, who holds the John H. Childers, M.D. Professorship in Pathology. Our findings suggest that these rare PAX7 cells are the key cells within the testes that are ultimately responsible for male fertility.

Importantly, even after exposure to toxic chemotherapy or radiation treatments, the PAX7-expressing cells continued to divide and thus could contribute to restoring sperm development.

First author Gina Aloisio, a student in UT Southwesterns Medical Scientist Training Program, is the recipient of a Fellowship Award from the UT Southwestern Cecil H. and Ida Green Center for Reproductive Biology Sciences. Other UT Southwestern researchers involved in the work include Dr. Kent Hamra, Assistant Professor of Pharmacology; Dr. James Amatruda, Associate Professor of Pediatrics, Internal Medicine, and Molecular Biology, the Horchow Family Scholar in Pediatrics and holder of the Nearburg Family Professorship in Pediatric Oncology Research; Dr. Anita Sengupta, Assistant Professor of Pathology; Dr. Ileana Cuevas, Instructor of Pathology; Dr. Yuji Nakada, Instructor of Pathology; Abhijit Bugde, Department of Cell Biology; graduate student researchers Hatice Saatcioglu, Christopher Pea, and Hema Manjunath; and former UT Southwestern researchers Dr. Michael Baker, Dr. Edward Tarnawa, and Jishnu Mukherjee.

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UT Southwestern Scientists Identify Rare Stem Cells in Testis That Hold Potential for Infertility Treatments

45 minutes ago by Bill Hathaway Separating the good stem cells from the bad. Credit: Matthew Chock, NYC

The promise of embryonic stem cell research has been thwarted by an inability to answer a simple question: How do you know a good stem cell from a bad one?

Yale researchers report in the Sept. 4 issue of the journal Cell Stem Cell that they have found a marker that predicts which batch of personalized stem cells will develop into a variety of tissue types and which will develop into unusable placental or tumor-like tissues.

Scientists have been unable to capitalize on revolutionary findings in 2006 that adult cells could be made young again with the simple introduction of four factors. Hopes were raised that doctors would soon have access to unlimited supplies of a patient's own iPSCsinduced pluripotent stem cellsthat could be used to repair many types of tissue damage. However, efforts to direct these cells to therapeutic goals have proved difficult. Many attempts to use cells clinically have failed because they form tumors instead of the desired tissue.

The team of Yale Stem Cell Center researchers led by senior author Andrew Xiao identified a variant histonea protein that helps package DNAwhich can predict the developmental path of iPSC cells in mice. An accompanying paper in the same journal by researchers at the Whitehead Institute at MIT and Hebrew University in Israel also identifies at different marker that also appears to predict stem cell fate.

"The trend is to raise the standards and quality very high, so we can think about using these cells in clinic," Xiao said. "With our assay, we have a reliable molecular marker that can tell what is a good cell and what is a bad one."

Explore further: New reprogramming factor cocktail produces therapy-grade induced pluripotent stem cells

Journal reference: Cell Stem Cell

Provided by Yale University

Induced pluripotent stem cells (iPSCs)adult cells reprogrammed back to an embryonic stem cell-like statemay hold the potential to cure damaged nerves, regrow limbs and organs, and perfectly model a ...

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How to tell good stem cells from the bad