TAG: "Stem cells"

Bone marrow stem cells show promise in stroke treatment


UC Irvine analysis reveals that they trigger repair mechanisms, limit inflammation.

Steven Cramer, UC Irvine

Stem cells culled from bone marrow may prove beneficial in stroke recovery, scientists at UC Irvine’s Sue & Bill Gross Stem Cell Research Center have learned.

In an analysis of published research, neurologist Dr. Steven Cramer and biomedical engineer Weian Zhao identified 46 studies that examined the use of mesenchymal stromal cells – a type of multipotent adult stem cells mostly processed from bone marrow – in animal models of stroke. They found MSCs to be significantly better than control therapy in 44 of the studies.

Importantly, the effects of these cells on functional recovery were robust regardless of the dosage, the time the MSCs were administered relative to stroke onset or the method of administration. (The cells helped even if given a month after the event and whether introduced directly into the brain or injected via a blood vessel.)

“Stroke remains a major cause of disability, and we are encouraged that the preclinical evidence shows [MSCs’] efficacy with ischemic stroke,” said Cramer, a professor of neurology and leading stroke expert. “MSCs are of particular interest because they come from bone marrow, which is readily available, and are relatively easy to culture. In addition, they already have demonstrated value when used to treat other human diseases.”

He noted that MSCs do not differentiate into neural cells. Normally, they transform into a variety of cell types, such as bone, cartilage and fat cells. “But they do their magic as an inducible pharmacy on wheels and as good immune system modulators, not as cells that directly replace lost brain parts,” he said.

In an earlier report focused on MSC mechanisms of action, Cramer and Zhao reviewed the means by which MSCs promote brain repair after stroke. The cells are attracted to injury sites and, in response to signals released by these damaged areas, begin releasing a wide range of molecules. In this way, MSCs orchestrate numerous activities: blood vessel creation to enhance circulation, protection of cells starting to die, growth of brain cells, etc. At the same time, when MSCs are able to reach the bloodstream, they settle in parts of the body that control the immune system and foster an environment more conducive to brain repair.

“We conclude that MSCs have consistently improved multiple outcome measures, with very large effect sizes, in a high number of animal studies and, therefore, that these findings should be the foundation of further studies on the use of MSCs in the treatment of ischemic stroke in humans,” said Cramer, who is also clinical director of the Sue & Bill Gross Stem Cell Research Center.

The analysis appears in the April 8 issue of Neurology. Quynh Vu, Kate Xie and Mark Eckert of UC Irvine contributed to the project, which received support from UC Irvine’s Institute for Clinical & Translational Science through the National Center for Research Resources (grant 5M011 RR-00827-29) and the National Institutes of Health (grants K24HD074722 and R01 NS059909).

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$6.5M gift establishes UC San Diego lab for regenerative ophthalmology


New lab at Shiley Eye Center will investigate advances to reverse vision loss, blindness.

A $6.5 million gift from a grateful patient will create the Richard C. Atkinson Laboratory for Regenerative Ophthalmology in the department of ophthalmology at the UC San Diego Shiley Eye Center. The new lab will investigate cell replacement therapies, tissue engineering and other biomedical advances to reverse vision loss and blindness. Work conducted at the lab will utilize novel stem cell approaches that are consistent with the vision of the newly created Sanford Clinical Stem Cell Center at UC San Diego, which was announced in late 2013.

“This significant gift will provide UC San Diego the foundation for innovation as researchers at the Shiley Eye Center employ a multidisciplinary approach that integrates ophthalmology, vision research, bioengineering, neurosciences and stem cell biology,” said UC San Diego Chancellor Pradeep K. Khosla.

The donor chose to name the laboratory in honor of Richard Atkinson, former University of California president and UC San Diego chancellor, for his lasting impact not only on UC San Diego, but also on the entire UC system. A professor emeritus of cognitive science and psychology, Atkinson served as president of the UC system from 1995 to 2003. Before becoming president, he served for 15 years as chancellor of UC San Diego. He is a former director of the National Science Foundation.

The UC San Diego department of ophthalmology at the Shiley Eye Center is the only academic eye center in the region offering the most advanced treatments across all areas of eye care. World-class clinicians, surgeons, scientists and staff are dedicated to excellence and providing the best possible patient care to prevent, treat and cure eye diseases. The center’s research is at the forefront of developing new methods for diagnosis and treatment of eye diseases and disorders.

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Stem cell findings may offer answers for some bladder defects, diseases


UC Davis discovery opens up opportunities using pluripotent cells.

Eric Kurzrock, UC Davis

For the first time, scientists have succeeded in coaxing laboratory cultures of human stem cells to develop into the specialized, unique cells needed to repair a patient’s defective or diseased bladder.

The breakthrough, developed at the UC Davis Institute for Regenerative Cures and published today (March 21) in the scientific journal Stem Cells Translational Medicine, is significant because it provides a pathway to regenerate replacement bladder tissue for patients whose bladders are too small or do not function properly, such as children with spina bifida and adults with spinal cord injuries or bladder cancer.

“Our goal is to use human stem cells to regenerate tissue in the lab that can be transplanted into patients to augment or replace their malfunctioning bladders,” said Eric Kurzrock, professor and chief of the division of pediatric urologic surgery at UC Davis Children’s Hospital and lead scientist of the study, which is titled “Induction of Human Embryonic and Induced Pluripotent Stem Cells into Urothelium.”

To develop the bladder cells, Kurzrock and his UC Davis colleagues investigated two categories of human stem cells. In their key experiments, they used induced pluripotent stem cells (iPS cells), which were derived from lab cultures of human skin cells and umbilical blood cells that had been genetically reprogrammed to convert to an embryonic stem cell-like state.

If additional research demonstrates that grafts of bladder tissue grown from human stem cells will be safe and effective for patient care, Kurzrock said that the source of the grafts would be iPS cells derived from a patient’s own skin or umbilical cord blood cells. This type of tissue would be optimal, he said, because it lowers the risk of immunological rejection that typifies most transplants.

In their investigation, Kurzrock and his colleagues developed a protocol to prod the pluripotent cells into becoming bladder cells. Their procedure was efficient and, most importantly, the cells proliferated over a long period of time – a critical element in any tissue engineering application.

“What’s exciting about this discovery is that it also opens up an array of opportunities using pluripotent cells,” said Jan Nolta, professor and director of the UC Davis Stem Cell program and a co-author on the new study. “When we can reliably direct and differentiate pluripotent stem cells, we have more options to develop new and effective regenerative medicine therapies. The protocols we used to create bladder tissue also provide insight into other types of tissue regeneration.”

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Grant supports research on the cause of childhood leukemia


UC Santa Cruz research could help enable the design of targeted cancer drugs.

Camilla Forsberg, UC Santa Cruz

Biomedical research at UC Santa Cruz has the potential to change how the most common type of childhood cancer is treated. A new grant from the nonprofit Alex’s Lemonade Stand Foundation will help UCSC researcher Camilla Forsberg advance her work to identify the root cause of acute lymphocytic leukemia (ALL) in infants and children.

Approximately 2,900 children and teens are diagnosed with ALL each year in the United States. Most are ages 2 to 3 years when diagnosed.

Forsberg, associate professor of biomolecular engineering in the Jack Baskin School of Engineering, and co-director for the UCSC Institute for the Biology of Stem Cells, is one of 16 researchers nationwide who have been awarded the foundation’s Innovations Awards. The two-year, $250,000 awards provide critical and significant seed funding for experienced investigators with novel and promising approaches to finding causes and cures for childhood cancers.

“Understanding the cause of this disease will enable the design of drugs that specifically eliminate cancer cells,” said Forsberg, “without causing damage to the body’s healthy cells while curing children with cancer.”

Avoiding treatment side effects is particularly important in children, as their growing bodies are much less able to tolerate standard chemotherapy. The idea of specific drug targeting is based on the success with the drug Gleevec in treating patients with chronic myelogenous leukemia.

Leukemia is a cancer that starts in early blood-forming cells. In a healthy child, the bone marrow makes blood stem cells (immature cells) that become mature blood cells over time. Cancer researchers like Forsberg are seeking a better understanding of what causes blood-forming stem cells to start behaving abnormally.

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Scientists transform skin cells into functioning liver cells


Study highlights novel reprogramming method, offers new hope for treating liver failure.

Sheng Ding

The power of regenerative medicine now allows scientists to transform skin cells into cells that closely resemble heart cells, pancreas cells and even neurons. However, a method to generate cells that are fully mature — a crucial prerequisite for life-saving therapies—has proven far more difficult. But now, scientists at the Gladstone Institutes and UC San Francisco have made an important breakthrough: they have discovered a way to transform skin cells into mature, fully functioning liver cells that flourish on their own, even after being transplanted into laboratory animals modified to mimic liver failure.

In previous studies on liver-cell reprogramming, scientists had difficulty getting stem cell-derived liver cells to survive once being transplanted into existing liver tissue. But the Gladstone-UCSF team figured out a way to solve this problem. Writing in the latest issue of the journal Nature, researchers in the laboratories of Gladstone Senior Investigator Sheng Ding, Ph.D., and UCSF Associate Professor Holger Willenbring, M.D., Ph.D., reveal a new cellular reprogramming method that transforms human skin cells into liver cells that are virtually indistinguishable from the cells that make up native liver tissue.

These results offer new hope for the millions of people suffering from, or at risk of developing, liver failure — an increasingly common condition that results in progressive and irreversible loss of liver function. At present, the only option is a costly liver transplant. So, scientists have long looked to stem cell technology as a potential alternative. But thus far they have come up largely empty-handed.

“Earlier studies tried to reprogram skin cells back into a pluripotent, stem cell-like state in order to then grow liver cells,” explained Ding, one of the paper’s senior authors, who is also a professor of pharmaceutical chemistry at UCSF, with which Gladstone is affiliated. “However, generating these so-called induced pluripotent stem cells, or iPS cells, and then transforming them into liver cells wasn’t always resulting in complete transformation. So we thought that, rather than taking these skin cells all the way back to a pluripotent, stem cell-like state, perhaps we could take them to an intermediate phase.”

This research, which was performed jointly at the Roddenberry Center for Stem Cell Research at Gladstone and the Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, involved using a “cocktail” of reprogramming genes and chemical compounds to transform human skin cells into cells that resembled the endoderm. Endoderm cells are cells that eventually mature into many of the body’s major organs—including the liver.

“Instead of taking the skin cells back to the beginning, we took them only part way, creating endoderm-like cells,” added Gladstone and CIRM postdoctoral scholar Saiyong Zhu, Ph.D., one of the paper’s lead authors. “This step allowed us to generate a large reservoir of cells that could more readily be coaxed into becoming liver cells.”

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New molecular ‘cocktail’ transforms skin cells into beating heart cells


Study represents important step toward therapies that regenerate heart muscle.

Sheng Ding

The power of regenerative medicine appears to have turned science fiction into scientific reality — by allowing scientists to transform skin cells into cells that closely resemble beating heart cells. However, the methods required are complex, and the transformation is often incomplete. But now, scientists at the UC San Francisco-affiliated Gladstone Institutes have devised a new method that allows for the more efficient — and, importantly, more complete — reprogramming of skin cells into cells that are virtually indistinguishable from heart muscle cells.

These findings, based on animal models and described in the latest issue of Cell Reports, offer newfound optimism in the hunt for a way to regenerate muscle lost in a heart attack.

Heart disease is the world’s leading cause of death, but recent advances in science and medicine have improved the chances of surviving a heart attack. In the United States alone, nearly 1 million people have survived an attack, but are living with heart failure — a chronic condition in which the heart, having lost muscle during the attack, does not beat at full capacity. So, scientists have begun to look toward cellular reprogramming as a way to regenerate this damaged heart muscle.

The reprogramming of skin cells into heart cells, an approach pioneered by Gladstone Investigator, Deepak Srivastava, M.D., has required the insertion of several genetic factors to spur the reprogramming process. However, scientists have recognized potential problems with scaling this gene-based method into successful therapies. So some experts, including Gladstone senior investigator Sheng Ding, Ph.D., have taken a somewhat different approach.

“Scientists have previously shown that the insertion of between three and seven genetic factors can result in a skin cell being directly reprogrammed into a beating heart cell,” explained Ding, the paper’s senior author and a professor of pharmaceutical chemistry at UCSF. “But in my lab, we set out to see if we could perform a similar transformation by eliminating — or at least reducing — the reliance on this type of genetic manipulation.”

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Genome editing goes hi-fi


Innovative technique in stem cells could boost scientists’ ability to study genetic disease.

Bruce Conklin

Sometimes biology is cruel. Sometimes simply a one-letter change in the human genetic code is the difference between health and a deadly disease. But even though doctors and scientists have long studied the often devastating disorders caused by these tiny changes, replicating these changes in the lab in order to study them in human stem cells has proven challenging. But now, scientists at the UC San Francisco-affiliated Gladstone Institutes have found a way to efficiently edit the human genome one letter at a time—not only boosting researchers’ ability to model human disease, but also paving the way for therapies that cure disease—by fixing these so-called ‘bugs’ in a patient’s genetic code.

Led by Gladstone investigator and professor in the UCSF School of Medicine, Bruce Conklin, M.D., the research team describes in an issue of Nature Methods how they have solved one of science and medicine’s most pressing problems: how to efficiently and accurately capture rare genetic mutations that cause disease—as well as how to fix them. This pioneering technique highlights the type of out-of-the-box thinking that is often critical for scientific success.

“Advances in human genetics have led to the discovery of hundreds of genetic changes linked to disease, but until now we’ve lacked an efficient means of studying them,” explained Conklin. “To meet this challenge, we must have the capability to engineer the human genome, one letter at a time, with tools that are efficient, robust and accurate. And the method that we outline in our study does just that.”

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Study represents important step toward a cure for type 1 diabetes


Scientists reprogram skin cells into insulin-producing pancreas cells.

Sheng Ding

A cure for type 1 diabetes has long eluded even the top experts. Not because they do not know what must be done—but because the tools did not exist to do it. But now scientists in the laboratory of Gladstone Institutes’ investigator Sheng Ding, M.D., Ph.D., harnessing the power of regenerative medicine, have developed a technique in animal models that could replenish the very cells destroyed by the disease. The team’s findings, published online today (Feb. 6) in the journal Cell Stem Cell, are an important step towards freeing patients from the life-long injections that characterize this devastating disease.

Type 1 diabetes, which usually manifests during childhood, is caused by the destruction of beta-cells (ß-cells). ß-cells are a type of cell that normally resides in the pancreas and produces a hormone called insulin. Without insulin, the body’s organs have difficulty absorbing sugars, such as glucose, from the blood. Once a death sentence, the disease can now be managed with regular glucose monitoring and insulin injections. A more permanent solution, however, would be to replace the missing ß-cells. But these cells are hard to come by, so researchers have looked towards stem cell technology as a way to make them.

“The power of regenerative medicine is that it can potentially provide an unlimited source of functional, insulin-producing ß-cells that can then be transplanted into the patient,” said Ding, who is also a professor at UC San Francisco, with which Gladstone is affiliated. “But previous attempts to produce large quantities of healthy ß-cells — and to develop a workable delivery system — have not been entirely successful. So we took a somewhat different approach.”

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Stem cell signal linked with cancer growth


Findings shed new light on the fundamental regulators of cell growth.

Tannishtha Reya, UC San Diego

Tannishtha Reya, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a protein critical to hematopoietic stem cell function and blood formation. The finding has potential as a new target for treating leukemia because cancer stem cells rely upon the same protein to regulate and sustain their growth.

Hematopoietic stem cells give rise to all other blood cells. Writing in the Feb. 2 advance online issue of Nature Genetics, principal investigator Tannishtha Reya, Ph.D., professor in the Department of Pharmacology, and colleagues found that a protein called Lis1 fundamentally regulates asymmetric division of hematopoietic stem cells, assuring that the stem cells correctly differentiate to provide an adequate, sustained supply of new blood cells.

Asymmetric division occurs when a stem cell divides into two daughter cells of unequal inheritance: One daughter differentiates into a permanently specialized cell type while the other remains undifferentiated and capable of further divisions.

“This process is very important for the proper generation of all the cells needed for the development and function of many normal tissues,” said Reya. When cells divide, Lis1 controls orientation of the mitotic spindle, an apparatus of subcellular fibers that segregates chromosomes during cell division.

“During division, the spindle is attached to a particular point on the cell membrane, which also determines the axis along which the cell will divide,” Reya said. “Because proteins are not evenly distributed throughout the cell, the axis of division, in turn, determines the types and amounts of proteins that get distributed to each daughter cell. By analogy, imagine the difference between cutting the Earth along the equator versus halving it longitudinally. In each case, the countries that wind up in the two halves are different.”

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UC researchers awarded stem cell grants


Basic biology awards total nearly $19M; UC also to participate in genomics center.

UC Santa Cruz's Josh Stuart will direct the data coordination and management program for the new Center of Excellence in Stem Cell Genomics.

UC Santa Cruz's Josh Stuart will direct the data coordination and management program for the new Center of Excellence in Stem Cell Genomics.

The University of California and its affiliates received 19 grants totaling nearly $19 million in the latest round of funding from the state’s stem cell agency, and two UC campuses will participate in a project awarded $40 million to create a Center of Excellence in Stem Cell Genomics.

The California Institute for Regenerative Medicine’s governing board warded a total of $67 million for this round of grants, funding the center of excellence and 27 basic biology research projects intended to form a foundation for future clinical advances. The basic biology projects include ones that will aid efforts to treat a range of ailments, from cancer to cartilage damage to heart disease.

The center will apply the powerful tools of genomics – studying the complete genetic makeup of a cell or organism – to stem cell research. The goal is to gain a deeper understanding of the disease processes in cancer, diabetes, heart disease and mental health, and ultimately to try to find safer and more effective ways of using stem cells in medical research and therapy. The center’s joint principal investigators are Stanford University and the Salk Institute for Biological Studies. UC San Diego, the Scripps Research Institute, the J. Craig Venter Institute and Illumina Inc. will collaborate on the project; UC Santa Cruz will run the data coordination and management component and receive about $5.4 million for its part in the center.

Lisa Flanagan, UC Irvine

Lisa Flanagan, UC Irvine

Overall, CIRM’s governing board has awarded around $1.8 billion in stem cell grants, with half of the total going to the University of California or UC-affiliated institutions.

Basic Biology V Awards:

  • UC Berkeley, $1.4 million: Andrew Dillin
  • UC Irvine, $1.5 million: Lisa Flanagan, Peter Donovan
  • UCLA, $3.5 million: Samantha Butler, Denis Evseenko, Thomas Otis, Lili Yang
  • UC Merced, $476,052: Kara McCloskey
  • UC San Diego, $8.2 million: David Cheresh, Lawrence Goldstein, Dianne McKay, Christian Metallo, Cornelis Murre, Maike Sander, Wei Wang, Miles Wilkinson
  • UC San Francisco, $2.4 million: Mark Anderson, Valerie Weaver
  • UCSF-affiliated Gladstone Institutes, $1.4 million: Sheng Ding

For more information:
CIRM release

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A giant step forward


UC Santa Barbara lab receives $1M to explore a new cell survival process named anastasis.

During anastasis, human cells recover from the brink of death. Top: HeLa cells stained blue to highlight DNA and red to label mitochondria before treatment with ethanol to induce apoptosis. The bottom panel shows (from left) untreated cells, ethanol-affected cells and washed cells that have fully recovered.

During anastasis, human cells recover from the brink of death. Top: HeLa cells stained blue to highlight DNA and red to label mitochondria before treatment with ethanol to induce apoptosis. The bottom panel shows (from left) untreated cells, ethanol-affected cells and washed cells that have fully recovered.

With the discovery of a novel cell process called anastasis, UC Santa Barbara biologist Denise Montell has taken a giant step forward in developing fundamentally new approaches to regenerative medicine.

Her research, which holds promise in establishing revolutionary therapies for the treatment of heart disease, degenerative diseases and cancer, has received a huge boost in the form of a $1 million grant from the W. M. Keck Foundation.

“The scope of the project is huge because this is a brand-new cellular process about which we know nothing,” said Montell, the Duggan Professor of Molecular, Cellular and Developmental Biology at UCSB. “We have to learn everything. It’s basically starting a whole new field.”

Anastasis is the process by which dying cells recuperate after trauma, thus overturning the dogma that cell death is irreversible. According to Montell, the mechanism likely evolved as a means of salvaging cells and limiting permanent tissue damage in response to transient injuries and stresses such as ischemia (deficient blood supply), radiation or toxins.

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Study discovers therapy to correct a severe chromosome defect


Induced pluripotent stem cell reprogramming offers potential to correct abnormal chromosomes.

Anthony Wynshaw-Boris

Anthony Wynshaw-Boris

Geneticists from Ohio, California and Japan joined forces in a quest to correct a faulty chromosome through cellular reprogramming. Their study, published online Jan. 12 in Nature, used stem cells to correct a defective “ring chromosome” with a normal chromosome. Such therapy has the promise to correct chromosome abnormalities that give rise to birth defects, mental disabilities and growth limitations.

“In the future, it may be possible to use this approach to take cells from a patient that has a defective chromosome with multiple missing or duplicated genes and rescue those cells by removing the defective chromosome and replacing it with a normal chromosome,” said senior author Anthony Wynshaw-Boris, M.D., Ph.D., James H. Jewell M.D. ’34 Professor of Genetics and chair of Case Western Reserve School of Medicine Department of Genetics and Genome Sciences and University Hospitals Case Medical Center.

Wynshaw-Boris led this research while a professor in pediatrics, the Institute for Human Genetics and the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UC San Francisco before joining the faculty at Case Western Reserve in June 2013.

Individuals with ring chromosomes may display a variety of birth defects, but nearly all persons with ring chromosomes at least display short stature due to problems with cell division. A normal chromosome is linear, with its ends protected, but with ring chromosomes, the two ends of the chromosome fuse together, forming a circle. This fusion can be associated with large terminal deletions, a process where portions of the chromosome or DNA sequences are missing. These deletions can result in disabling genetic disorders if the genes in the deletion are necessary for normal cellular functions.

The prospect for effective countermeasures has evaded scientists — until now. The international research team discovered the potential for substituting the malfunctioning ring chromosome with an appropriately functioning one during reprogramming of patient cells into induced pluripotent stem cells (iPSCs). iPSC reprogramming is a technique that was developed by Shinya Yamanaka, M.D., Ph.D., a co-corresponding author on the Nature paper. Yamanaka is a senior investigator at the UCSF-affiliated Gladstone Institutes, a professor of anatomy at UCSF, and the director of the Center for iPS Cell Research and Application (CiRA) at the Institute for Integrated Cell-Material Sciences (iCeMS) in Kyoto University. He won the Nobel Prize in Medicine in 2012 for developing the reprogramming technique.

Marina Bershteyn, Ph.D., a postdoctoral fellow in the Wynshaw-Boris lab at UCSF, along with Yohei Hayashi, Ph.D., a postdoctoral fellow in the Yamanaka lab at the Gladstone Institutes, reprogrammed skin cells from three patients with abnormal brain development due to a rare disorder called Miller-Dieker Syndrome, which results from large terminal deletions in one arm of chromosome 17. One patient had a ring chromosome 17 with the deletion, and the other two patients had large terminal deletions in one copy of chromosome 17, but not a ring. Additionally, each of these patients had one normal chromosome 17.

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