Category Archives: Stem Cells

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Associate Professor Akira Shimamoto and Professor Hidetoshi Tahara at the Graduate School of Biomedical & Health Science in Hiroshima University, Professor Koutaro Yokote at the Graduate School of Medicine in Chiba University, Visiting Professor Makoto Goto at the Medical Center East in Tokyo Women's Medical University, and collaborators including the staff at the Cancer Chemotherapy Center in the Japanese Foundation for Cancer Research, Tottori University, and Keio University established induced pluripotent stem (iPS) cells from the fibroblasts of Werner Syndrome patients.

These results were published in PLOS ONE in an article entitled "Reprogramming Suppresses Premature Senescence Phenotypes of Werner Syndrome Cells and Maintains Chromosomal Stability over Long-Term Culture."

Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. This syndrome occurs frequently in Japan, affecting 1 in 20,000 to 1 in 40,000 people. The therapeutic methods for this disease are very limited and it is expected that iPS cells can be used for the development of innovative therapies.

Dr. Shimamoto and his collaborators analyzed patient-derived iPS cells and found that telomeric abnormalities in the fibroblasts of these patients, which were caused by the lack of WRN helicase encoded by the gene responsible for Werner syndrome, were recovered in the iPS cells generated from these patients. Furthermore, Dr. Shimamoto found that the expression levels of aging-related genes, including those encoding cell cycle inhibitors and inflammatory cytokines, in the patient-derived iPS cells were the same as those in normal iPS cells, even though the expression levels of these genes in the fibroblasts of the patients were higher than those in normal fibroblasts.

Dr. Shimamoto said, "So far, the use of patient cells was restricted to blood or dermal cells in basic research. The iPS cells that we have established will provide an opportunity for drug discovery for the treatment of Werner syndrome and also help with better understanding of the mechanism of this disease. In addition, the mutated WRN gene in patient-derived iPS cells can be corrected by genome editing. This advantage will be help in the development of new gene and cell therapies for Werner syndrome."

Explore further: Scientists find that SCNT derived cells and IPS cells are similar

Journal reference: PLoS ONE

Provided by Hiroshima University

A team led by New York Stem Cell Foundation (NYSCF) Research Institute scientists conducted a study comparing induced pluripotent stem (iPS) cells and embryonic stem cells created using somatic cell nuclear transfer (SCNT). ...

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Establishment of induced pluripotent stem cells from Werner syndrome fibroblasts

ANTI AGEING - WHAT ARE HOW WE USE STEM CELLS
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ANTI AGEING - WHAT ARE & HOW WE USE STEM CELLS - Video

PUBLIC RELEASE DATE:

17-Nov-2014

Contact: Nik Papageorgiou n.papageorgiou@epfl.ch 41-216-932-105 Ecole Polytechnique Fdrale de Lausanne @EPFL_en

Chronic myeloid leukemia develops when a gene mutates and causes an enzyme to become hyperactive, causing blood-forming stem cells in the bone marrow to grow rapidly into abnormal cells. The enzyme, Abl-kinase, is a member of the "kinase" family of enzymes, which serve as an "on" or "off" switch for many functions in our cells. In chronic myeloid leukemia, the hyperactive Abl-kinase is targeted with drugs that bind to a specific part of the enzyme and block it, aiming to ultimately kill the fast-growing cancer cell. However, treatments are often limited by the fact that the cancer cells can adapt to resist drugs. EPFL scientists have identified an alternative part of Abl-kinase on which drugs can bind and act with a reduced risk of drug resistance. Their work is published in Nature Communications.

Abl-kinase and leukemia

Abl-kinase can turn "on" molecules that are involved in many cell functions including cell growth. In chronic myeloid leukemia, the chromosome that contains the gene for Abl-kinase swaps a section with another chromosome, causing what is known as the "Philadelphia chromosome". When this mutation takes place in the blood stem cells in the bone marrow, Abl-kinase fuses with another protein, turning into a deregulated, hyperactive enzyme. This causes large numbers of blood-forming stem cells to grow into an abnormal type of white blood cell, which gives rise to chronic myeloid leukemia.

To treat this type of leukemia we use drugs that specifically bind and block a part of Abl-kinase called the "active site". As the name suggests, this is the part of the enzyme that binds molecules to turn them on. Therefore, blocking the active site with a drug stops the hyperactivity of Abl-kinase caused by the Philadelphia mutation and slow down or even abolishes the production of abnormal cancerous blood cells. The problem is that targeting the active site of Abl-kinase often causes the cancer cells to adapt and develop drug resistance, making them harder to kill.

An indirect path against resistance

A team of researchers led by Oliver Hantschel at EPFL (ISREC) has now discovered a new way to indirectly inhibit the activity of Abl-kinase. The scientists systematically made small, strategic mutations to Abl-kinase that caused its 3D structure to change. Then they tested each mutant version of the enzyme to see if its function would change.

Hantschel's team built on previous studies showing that Abl-kinase is indirectly controlled by another part of itself called the "SH2 region", which is located close to the active site. Normally, the SH2 region regulates the active site by opening and closing it. But under the Philadelphia mutation, that regulation is lost. What the scientists discovered was that when the Philadelphia mutation takes effect, the SH2 region actually "clamps" open the active site of Abl-kinase and forces it to go into overdrive.

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A new approach to fighting chronic myeloid leukemia

What is a Stem Cell Support Serum? | RG Cell | Agerite Solutions
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Nov. 13, 2014

One remarkable quality of pluripotent stem cells is they are immortal in the lab, able to divide and grow indefinitely under the right conditions. It turns out this ability also may exist further down the development path, with the workhorse progenitor cells responsible for creating specific tissues.

A team from the Morgridge Institute for Research regenerative biology group, led by University of Wisconsin-Madison professor and stem cell pioneer James Thomson, discovered a way to impose an immortal-like state on mouse progenitor cells responsible for producing blood and vascular tissue. By regulating a small number of genes, the cells became "trapped" in a self-renewing state and capable of producing functional endothelial, blood and smooth muscle cells.

David Vereide

The finding, to be published in the December 9, 2014 issue of Stem Cell Reports, points to a potential new approach to developing cells in the lab environment for use in drug screening, therapies and as a basic research tool.

"The biggest takeaway for me is the ability to arrest development of these cells," says David Vereide, a Morgridge fellow in regenerative biology and lead author on the paper. "Normally, these cells are ephemeral and get used up while differentiating into specific cell types, but we found a way to interrupt that."

During development, blood and vascular cells are thought to originate from a progenitor cell known as a hemangioblast. This research project identified and imposed six transcription factors on the cells that allowed hemangioblasts to keep proliferating over multiple generations. Transcription factors are proteins that regulate which genes get turned on or off in a genome.

In this case, the transcription factors act to "keep the lights on" in these cellular factories that kept them dividing and expanding, he says.

One exciting element of this research, Vereide says, is it could greatly improve the efficiency of creating cell types that have research and therapeutic value. Progenitor cells, the "sons and daughters" of stem cells that give rise to specific tissue, are usually the end steps in producing the key building-block cells for the body brain, vasculature, bone, etc.

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Morgridge scientists find way to keep the lights on for cell self-renewal

UW-Madison cell and regenerative biology professor James Thomson and his team of scientists recently made new strides in their extensive stem cell research.

Thomson and his team members from the Morgridge Institute for Research conducted tests and experiments on mice to advance their research, according to a UW-Madison news release.

Results from the trials led to a developed method which eternally preserves progenitor cells in their pluripotent stages. In other words, the stem cells, which eventually transform into specific tissues, will forever remain in a phase with the potential to become one of at least 200 different cell types.

Maintaining pluripotent stem cells in a controlled environment enables them to undergo constant reproduction. The cells will cyclically divide and grow to produce working endothelial, blood and smooth muscle cells.

David Vereide, one of Thomsons associates at MIR, said the cells are able to self-renew through the regulation of a small quantity of genes.

"Normally, these cells are ephemeral and get used up while differentiating into specific cell types, but we found a way to interrupt that, Vereide explained in the release.

He also said their findings bring researchers very close to finalizing medical uses for stem cells.

Thomson said in the release he and his team have ambitions to progress from examining mouse cells to working with human cells, and motivate other experts to uncover even more valuable information on the topic.

"I'm hoping that other scientists who see this get inspired," Vereide said in the release. "If you dig into the progenitor state of any tissue, you will probably find core factors that will drive the expansion of those progenitors in a dish.

The new discovery will be recorded in the Dec. 9 publication of Stem Cell Reports.

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UW-Madison researchers discover method to encourage self-renewal of stem cells

A research team led by Jackson Laboratory Professors Frank McKeon, Ph.D., and Wa Xian, Ph.D., reports on the role of certain lung stem cells in regenerating lungs damaged by disease.

The work, published Nov. 12 in the journal Nature, sheds light on the inner workings of the still-emerging concept of lung regeneration and points to potential therapeutic strategies that harness these lung stem cells.

"The idea that the lung can regenerate has been slow to take hold in the biomedical research community," McKeon says, "in part because of the steady decline that is seen in patients with severe lung diseases like chronic obstructive pulmonary disease (known as COPD) and pulmonary fibrosis."

Nevertheless, he notes, there are examples in humans that point to the existence of a robust system for lung regeneration. "Some survivors of acute respiratory distress syndrome, or ARDS, for example, are able to recover near-normal lung function following significant destruction of lung tissue."

Mice appear to share this capacity. Mice infected with the H1N1 influenza virus show progressive inflammation in the lung followed by outright loss of important lung cell types. Yet over several weeks, the lungs recover, revealing no signs of the previous lung injury.

Using this mouse model system, McKeon and his colleagues had previously identified a type of adult lung stem cell known as p63+/Krt5+ in the distal airways. When grown in culture, these lung stem cells formed alveolar-like structures, similar to the alveoli found within the lung. (Alveoli are the tiny, specialized air sacs that form at the ends of the smallest airways, where gas exchange occurs in the lung.) Following infection with H1N1, these same cells migrated to sites of inflammation in the lung and assembled into pod-like structures that resemble alveoli, both visually and molecularly.

In the new paper, the research team reports that the p63+/Krt5+ lung stem cells proliferate upon damage to the lung caused by H1N1 infection. Following such damage, the cells go on to contribute to developing alveoli near sites of lung inflammation.

To test whether these cells are required for lung regeneration, the researchers developed a novel system that leverages genetic tools to selectively remove these cells from the mouse lung. Mice lacking the p63+/Krt5+ lung stem cells cannot recover normally from H1N1 infection, and exhibit scarring of the lung and impaired oxygen exchange--demonstrating their key role in regenerating lung tissue.

The research team also showed that when individual lung stem cells are isolated and subsequently transplanted into a damaged lung, they readily contribute to the formation of new alveoli, underscoring their capacity for regeneration.

In the U.S. about 200,000 people have ARDS, a disease with a death rate of 40 percent, and there are 12 million patients with COPD. "These patients have few therapeutic options today," Xian says. "We hope that our research could lead to new ways to help them."

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Lung regeneration mechanism discovered

PUBLIC RELEASE DATE:

12-Nov-2014

Contact: Joyce Peterson joyce.peterson@jax.org 207-288-6058 Jackson Laboratory @jacksonlab

A research team led by Jackson Laboratory Professors Frank McKeon, Ph.D., and Wa Xian, Ph.D., reports on the role of certain lung stem cells in regenerating lungs damaged by disease.

The work, published Nov. 12 in the journal Nature, sheds light on the inner workings of the still-emerging concept of lung regeneration and points to potential therapeutic strategies that harness these lung stem cells.

"The idea that the lung can regenerate has been slow to take hold in the biomedical research community," McKeon says, "in part because of the steady decline that is seen in patients with severe lung diseases like chronic obstructive pulmonary disease (known as COPD) and pulmonary fibrosis."

Nevertheless, he notes, there are examples in humans that point to the existence of a robust system for lung regeneration. "Some survivors of acute respiratory distress syndrome, or ARDS, for example, are able to recover near-normal lung function following significant destruction of lung tissue."

Mice appear to share this capacity. Mice infected with the H1N1 influenza virus show progressive inflammation in the lung followed by outright loss of important lung cell types. Yet over several weeks, the lungs recover, revealing no signs of the previous lung injury.

Using this mouse model system, McKeon and his colleagues had previously identified a type of adult lung stem cell known as p63+/Krt5+ in the distal airways. When grown in culture, these lung stem cells formed alveolar-like structures, similar to the alveoli found within the lung. (Alveoli are the tiny, specialized air sacs that form at the ends of the smallest airways, where gas exchange occurs in the lung.) Following infection with H1N1, these same cells migrated to sites of inflammation in the lung and assembled into pod-like structures that resemble alveoli, both visually and molecularly.

In the new paper, the research team reports that the p63+/Krt5+ lung stem cells proliferate upon damage to the lung caused by H1N1 infection. Following such damage, the cells go on to contribute to developing alveoli near sites of lung inflammation.

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Jackson Laboratory researchers discover lung regeneration mechanism

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CHENNAI: It is harder for natives of Tamil Nadu to find a matching donor for a stem cell transplant compared to other states in the country. The suspected villain: Their genes.

A study published recently in British medical journal 'The Lancet' found that the likelihood of finding a matching stem cell donor for patients with blood-related problems in Tamil Nadu is 44.2% provided the registry had 10 lakh donors. The situation is the opposite in Haryana, with people in that state having the best chances (81.2%) of finding a donor.

Experts say consanguineous marriages are to blame. Consanguineous marriages increase the chances of patients finding a match within their small community but limit the possibility of finding one from a general donor pool.

"Unlike in other countries, stem cell variation in India is complex and dependent on ethnic variation," said Dr Dolly Daniel, professor of the department of transfusion medicine at Christian Medical College, Vellore, who was party of the study team. "Our aim was to find the size and genetic composition of each region and its impact on the proportion of patients who will be able to ?nd a suitable match."

She said Tamil Nadu could be at the tail-end of the list of states they surveyed because of inbreeding and a limited number of donors.

Stem cells are used to regenerate and repair diseased or damaged tissues. Adult stem cells are drawn from bone marrow, blood and the umbilical cord and are used to treat blood-related ailments like leukemia, thalassemia and as well as immunodeficiency.

The possibility of finding a matching stem cell donor within the family is around 30%.

"Finding a matching stem cell donor for the remaining 70% is a complex process. Most seek a graft from registries of unrelated adult donors or banked umbilical cord blood units," said Dr P Srinivasan, co-founder and chairman of Jeevan Stem Cell Bank.

Although the India stem cell industry is estimated to touch $540 million (Rs 3,250 crore) by 2015, the study noted that in terms of the number of donors, India has lagged in meeting demand. The study surveyed 10 adult donor and umbilical cord bank registries and clinical transplant centres in India and studied stem cells of 26 239 individuals.

The possibility of finding a perfect match within India is an average of 14.4% for a registry size of 25,000 and touches 60.6% for a size of 10 lakh. Registries in the country currently have around 1 lakh donors. The study said only when Indian registries have more than 2 lakh donors would patients have a good chance of finding the right match.

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Toughest for Tamil Nadu patients to get donor stem cells