Researchers hope one day to use stem cells in ways that cure spinal cord injuries, Parkinson’s disease and other ailments.

Stem cells are cells with the capacity to turn into any other type of human cell, be it bone, muscle or nerve cell.

Scientists have shown that the damage caused to nerve cells in multiple sclerosis could be reversed by activating stem cells in the body. The work on animal models of the disease improves our understanding of the devastating condition and may lead to treatments that regenerate the nervous system.

Stem cells are the body’s master cells, that can turn themselves into different types of mature cells given the right conditions.

Medistem Inc. (PINKSHEETS: MEDS) announced today publication of a peer reviewed paper describing the scientific rationale and preliminary results of three patients with multiple sclerosis treated with their own fat derived stem cells.

“In addition to our endometrial regenerative cell (ERC) universal donor stem cell technology, for which an IND has been filed, Medistem has been committed to developing a pipeline of therapeutic products, including in the area of immune modulation,” said Thomas Ichim, CEO of Medistem. “Given our previous observations and IP filings that a stem cell-rich component of adipose tissue, called the Stromal Vascular Fraction, can concurrently immune modulate, while inducing regenerative activities, we are pleased to see the clinical translation of this approach into multiple sclerosis patients.”

Multiple sclerosis affects approximately 400,000 Americans and is characterized by immunological attack on the myelin sheath that surrounds the core of the nerve fibers and facilitates the transmission of nerve impulses in the nervous system. Currently, use of stem cells for this disease involves extraction of bone marrow and suppression of the patient’s immune system. The therapy described in the publication circumvents the need for immune suppression and uses a simple liposuction procedure that is currently performed in thousands of plastic surgery clinics worldwide.

“Our collaborator in this publication, Dr. Robert Harman, CEO of Vet-Stem (www.vet-stem.com), has treated over 3,500 horses and 1,500 dogs with fat derived stem cells for inflammatory conditions such as osteoarthritis immune-mediated polyarthritis. The current work is an excellent example of veterinary findings being translated into human medicine,” stated Dr. Boris Minev, faculty at the University of California San Diego, who was senior author of the paper.

The article, titled “Non-expanded adipose stromal vascular fraction cell therapy for multiple sclerosis,” appeared today in the Journal of Translational Medicine , and was a collaboration between scientists and clinicians from Medistem; the University of Western Ontario; Hospital CIMA, San Jose, Costa Rica; Indiana University; Cell Medicine Institutes; University of California, San Diego; and University of Utah.

View entire article here: http://www.medicalnewstoday.com/articles/147531.php

The researchers pushed the stem cells to grow into critical nervous system support cells called oligodendrocytes, according to a report released Thursday.

Oligodendrocytes produce the myelin sheath that surrounds nerve fibers like wire insulation. The findings represent an important step toward embryonic stem cell-based therapies in general, experts say, and also for cell-based therapies for myelination disorders such as MS in particular. At the very least, the findings should lead to a laboratory model of the illness’ pathology.

“They are definitely laying the groundwork for being able to apply these cells in terms of a therapeutic application,” said Timothy Coetzee, executive director of Fast Forward, a wholly-owned subsidiary of the National Multiple Sclerosis Society, which partially funded the study.

Yet at the same time, he added, “It illustrated for me the critical importance of not assuming that because you can do something with a mouse cell, that a human cell is going to behave in the same manner.”

The research was published in the May issue of the journal Development.

At the heart of this study is a fundamental question: What’s the difference between mouse and man?

It’s not as silly as it sounds. Human experimentation being both morally and legally forbidden, researchers often use model organisms such as mice as proxies for human development. The underlying assumption, of course, is that these organisms have fundamentally the same biology as we do. Sometimes, though, that assumption turns out to be wrong.

For years, researchers using mouse embryonic stem cells (ESCs) knew that if they added one of two proteins, FGF2 or SHH, to the cells’ growth media, they could reliably induce those cells to become oligodendrocytes. The human application was obvious: ESC-derived oligodendrocytes could either be used directly as a cell therapy for MS and related diseases, or serve as research tools to study them.

But, when Dr. Su-Chun Zhang of the University of Wisconsin, Madison, who has been studying oligodendrocytes and myelination for nearly a quarter-century, tried to apply the culture conditions painstakingly worked out in rodents to human cells, oligodendrocytes failed to emerge.

“When we expand these [rodent] progenitor cells with FGF2 (and another factor called PDGF), these progenitor cells will become oligodendrocytes,” Zhang said. But, “What we discovered was that when we did [the experiment] in the same way with human progenitor cells, they were blocked in this process.”

By carefully dissecting the molecular events that occur as human ESCs differentiate first into neural stem cells, then neural progenitor cells, then pre-oligodendrocytes, and finally mature oligodendrocytes, Zhang and his team identified the source of the difference: While both rodents and humans control the process with the same regulatory circuitry and use the same molecules (including both FGF2 and SHH), FGF2 behaves differently in each species.

In mice, FGF2 promotes oligodendrocyte maturation; in humans, it inhibits the process.

“This finding is actually quite significant scientifically,” said Zhang, “because even [though] the transcriptional network is more or less the same, yet they respond to the same factor in an opposite way. To me, that’s quite extraordinary.”

Once that simple fact was understood, the experiment could be tweaked so that human embryonic stem cells could, in fact, generate oligodendrocytes.

The study, said Coetzee, “just reinforces the absolute importance of being able to do some of this very fundamental biology and fundamental understanding of what human cells do, before you start experimenting with them to put them into people.”

Dr. William Sheremata is professor of neurology at the University of Miami Miller School of Medicine. He sees many MS patients in his practice and called the study “an excellent example of work that is very carefully done by an expert group of people who really know what they are doing. So I think that the conclusion that FGF2 does not work to facilitate maturation of pre-oligodendrocytes is acceptable at face value. It is the first paper that has stated just that.”

Sheremata questioned the therapeutic implications of the report, however, suggesting that therapies based on “autologous stem cells” (adult stem cells) were more likely to bear fruit.

Coetzee, though, called the findings “absolutely critical” to moving toward clinical applications for MS, whether directly by injection of mature oligodendrocytes or more primitive precursor cells, because it both enables researchers to grow large quantities of these cells and to molecularly define the process by which that happens.

“This actually begins to lay the foundation for envisioning having the ability to create the mass quantities of stem cells that you’d need in order to have a therapeutic application in MS,” he said.

View entire post here: http://www.forbes.com/feeds/hscout/2009/04/09/hscout625910.html

Thursday, 9 April 2009 Wendy Zukerman
ABC

Mice with a human equivalent of multiple sclerosis have been successfully treated using genetically modified stem cells, say a group of Australian researchers.

The work, led by Dr James Chan of Monash University’s Centre of Inflammatory Diseases, may lead to the development of a similar technique to treat autoimmune diseases in humans.

Autoimmune diseases, such as type 1 diabetes and multiple sclerosis, are caused when immune cells, called T cells, incorrectly identify proteins created by the body as foreign objects, such as bacteria, and attack them.

To prevent these rogue T cells from entering the bloodstream, the immune system lures them with ‘self-proteins’ while they are developing in the thymus. T cells that bind tightly to these self-proteins are destroyed by the body’s immune system.

Some slip through this ‘net’ and for some people result in auto-immune disease.

Fully recovered

Chan and colleagues genetically modified a specific type of stem cell, which produce more self-protein to ensure that dangerous T cells are more effectively removed from the system.

In the study, which appeared in the Journal of Immunology, mice were inoculated to develop experimental autoimmune encephalomyelitis (EAE), the human equivalent of multiple sclerosis. The genetically modified stem cells were then transplanted into the mice.

“After the transplantation, the mice are completely resistant to disease,” says Chan.

While initial results are promising, Chan says human clinical trials would not be possible for some time.

“Before we transplant the stem cells we wipe out the immune system of the mice using high doses irradiation,” says Chan.

He says this level of irradiation would not suitable for humans.

The team is now looking at ways of overcoming the need for radiation, in order to make the procedure clinically viable.

Promising

Dr Carola Vinuesa of the John Curtin School of Medical Research at the Australian National University in Canberra, says the results are “very exciting and potentially very promising.”

But Vinuesa cautions that it is unclear how well the mouse model relates to human disease.

“The EAE mouse model of multiple sclerosis is not a model in which autoimmune disease develops spontaneously, as occurs with multiple sclerosis in humans,” she says.

She adds there is still a lot we don’t know about how healthy T cells know not to attack self-proteins.

“The mechanism by which they do this is still unclear, but the results [from this study] are spectacular,” says Vinuesa.

View entire post here: http://www.abc.net.au/science/articles/2009/04/09/2539614.htm?site=science&topic=latest

By JONATHAN MARTIN | 3/9/09 12:11 PM EDT Updated: 3/9/09 3:43 PM EDT

President Barack Obama Monday rescinded the Bush administration’s limits on federal funding for embryonic stem cell research and chided his predecessor for putting politics ahead of science.

Obama also signed an order meant to put scientific research back in the forefront in government decision-making.

“It is about ensuring that scientific data is never distorted or concealed to serve a political agenda — and that we make scientific decisions based on facts, not ideology,” Obama said. He won loud applause and even a few cheers from scientists who joined him in the East Room ceremony.

Many on the left and in the scientific community believe that, from stem cells to climate change, George W. Bush manipulated or ignored data and research for political purposes.

But it is Obama’s move to lift limits on stem cell research that has reignited one of the country’s central ethical debates.

Bush restricted the use of federal funding on stem cells, except for those already in existence at the time of his 2001 order. Obama’s move would clear the way for a big increase in federal funding for the research.

“At this moment, the full promise of stem cell research remains unknown, and it should not be overstated,” Obama said. “But scientists believe these tiny cells may have the potential to help us understand, and possibly cure, some of our most devastating diseases and conditions.”

By lifting the ban, Obama offers what many scientists think could be the path to a breakthrough in the search for the causes and cures of afflictions such as Parkinson’s disease, spinal cord damage or Alzheimer’s disease.

Polls also show public support for embryonic stem cell research, something the president alluded to in citing a “consensus” for his move.

Yet many conservatives see embryonic research as tantamount to the destruction of human life. Harvesting the stem cells requires the destruction of embryos, which are usually recovered from fertility clinics.

Obama called the debate “a false choice between sound science and moral values. In this case, I believe the two are not inconsistent. As a person of faith, I believe we are called to care for each other and work to ease human suffering.”

Obama directed the National Institutes of Health to set new research guidelines within 120 days.

Some Republicans agree with him, most notably Nancy Reagan.

“I’m very grateful that President Obama has lifted the restrictions on federal funding for embryonic stem cell research,” the former first lady said in a statement. “These new rules will now make it possible for scientists to move forward.”

But the anti-abortion community — a group which Obama courted during his campaign — made clear its anger.

“It is a sad day when the federal government will fund research that exploits living members of the human species as raw material for research,” said Douglas Johnson, a spokesman for the National Right to Life Committee, who added that the move puts the country on a “very steep, very slippery slope” toward cloning.

Obama, in his usual effort to blunt such ideological differences, sought to pre-empt that argument in his remarks, promising strict rules and saying his order would not allow a move toward human cloning.

“It is dangerous, profoundly wrong, and has no place in our society, or any society,” he said of cloning.

View this article at: http://www.politico.com/news/stories/0309/19785.html