Showing posts with label Stem-Cells. Show all posts
Showing posts with label Stem-Cells. Show all posts

Tuesday, May 13, 2008

Decoding Muscle Stem Cell Development

(HealthDay News) -- Muscle stem cells can't grow into mature muscle cells if there aren't enough nutrients, according to a study that offers new insight into how developing muscle cells sense and respond to nutrient levels.

The research, part of ongoing investigations into the effects of caloric restriction on physiology and aging, may help in the development of new treatments for muscle wasting.

In this study, National Institutes of Health researchers examined how the availability of glucose affects the ability of muscle stem cells (myoblasts) to develop into mature skeletal muscle fibers.

According to a news release about the study, the researchers "found that glucose restriction (GR) impaired differentiation of skeletal myoblasts and activated AMP-activated protein kinase (AMPK). These results define a pathway in which activation of AMPK in response to low glucose levels stimulates expression of the NAD+ biosynthetic enzyme Nampt. NAD+ is a known co-factor of SIRT1, which plays an important role in numerous physiological processes, including differentiation of skeletal muscle cells, and has been implicated in regulation of life span and aging. Importantly, inhibition of AMPK, Nampt or SIRT1 resulted in skeletal muscle cells that were oblivious to a nutrient-poor environment and were able to differentiate under conditions that otherwise would not be suitable."

The researchers said their findings, published in the May issue of Developmental Cell, show that a specific pathway controls muscle cell differentiation in response to low nutrient levels.

"We speculate that, functioning as a cellular checkpoint, the AMPK-Nampt-SIRT1 pathway may be activated by reduced nutrient availability to prevent cells from undertaking energy-demanding processes -- such as cell differentiation -- during calorie-unfavorable conditions. On the other hand, once nutrients become available, the pathway is inactivated to allow resumption of physiological development," researcher Vittorio Sartorelli said in a prepared statement.

This same mechanism also operates in adult tissues, which means it would be part of the response to a diet with reduced calorie intake. The researchers also found that both glucose restriction or treatment of skeletal muscle cells with metformin (a drug used to treat type 2 diabetes) had similar outcomes and activated SIRT1.

"It is therefore possible that the well-known benefits that diabetics derive from lowering the calorie intake in their diet may be attributable to activation of the AMPK-Nampt-SIRT1 axis," Sartorelli said.

He added that AMPK and SIRT1 may prove good targets for treatment of muscle-wasting.

More information
The U.S. National Institutes of Health has more about stem cells.

Saturday, April 26, 2008

Stem cell research harnessed for anti-aging remedies

Posted in Stem Cell Research on Fri April 25, 2008

National Stem Cell has revealed that it is set to launch a new range of anti-aging products that have been developed using stem cell research.

Tropelastin produced by human embryonic stem cells has been utilised by the company's subsidiary Decouverte Cosmetique in skin firming products, CosmeticsDesign.com reports.

Chief executive of National Stem Cell Michael Cohen told the website that it is this chemical that can provide women with a 'glow' after they conceive.

He added that the company had used pre-2001 stem cells and neither destroyed nor created any cells during product development.

Some scientists have criticised the use of stem cell research in the development of cosmetic products because they say the technology is not yet advanced enough to deliver drastic results.

"The notion that you could do that with a cream is a little bit ahead of itself," dermatologist Dr Kenneth Beer told the LA Times. "It's a great piece of marketing because there is so much interest in stem cells."

Tuesday, April 15, 2008

Heart's Stem Cells Not Created Equally

(HealthDay News) -- Not all heart cells are created by the same universal signal, a discovery that could lead to future treatments for congenital heart disease and heart attacks, U.S researchers say.

Experiments conducted on frogs challenge long-held beliefs that the stem cells that eventually develop into the heart's muscle tissue do so in reaction to the same cue.

"Not only does it tell us about how stem cells differentiate to create the heart, but it provides us with knowledge that may very well help us to repair heart muscle after a heart attack," researcher Dr. Cam Patterson, director of the Carolina Cardiovascular Biology Center at the University of North Carolina at Chapel Hill, said in a prepared statement.

The study was published online in the April 14 issue of the journal Developmental Cell and in the April 15 print edition.

The researchers manipulated genetic material in frog embryos so their cells would not produce a gene known as CASTOR, which had been linked to stem cell differentiation in the fruit fly.

Without CASTOR present, a small subset of cells at the base of an embryo's heart remained in a state of infancy while others developed. These infant cells, or progenitors, were later found to have developed into the outer walls of the heart's ventricles if they were allowed to progress normally.

This finding affects theories about the possibility of transplanting progenitor cells into the damaged area of the organ, such as heart-attack scarred muscle, in hope of creating healthy tissue. The theory supposes that all progenitors are the same.

"What we have found is that this belief simply isn't true," study senior author Frank Conlon, assistant professor of genetics in the UNC School of Medicine, said in a prepared statement. "Instead, there appear to be at least two types of progenitors, and we think there may be many more."

Conlon is now attempting to manipulate other genes in addition to CASTOR to determine how many types of heart cell progenitors exist. He hopes to verify his findings other animal models before searching for genetic counterparts in humans.

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