STANFORD, Calif. - Communication is critical. Garbled in, garbled out, so to (mis-)speak. Workers who get incomplete instructions produce an incomplete product, and that's exactly what happens with the stem cells in our aging muscles, according to researchers from the Stanford University School of Medicine.
Their study found that, as we age, the lines of communication to the stem cells of our muscles deteriorate and, without the full instructions, it takes longer for injured muscles to heal. Even then, the repairs aren't as good. But now that the researchers have uncovered the conduit that conveys the work orders to muscle stem cells, that knowledge could open the door to new therapies for injuries in a host of different tissues.
The key to the whole process is Wnt, a protein traditionally thought to help promote maintenance and proliferation of stem cells in many tissues. But in this instance, Wnt appears to block proper communication.
"That was a total surprise," said Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences. "We had no idea that the Wnt signaling pathway would have a negative effect on stem cell function." Rando, who also does research and clinical work at the Veterans Affairs Palo Alto Health Care System, is senior author of the research that will be published in the Aug. 10 issue of Science.
Rando said many drugs can block Wnt signaling. "Theoretically, given the number of ways to block Wnt and Wnt signaling, one could envision this becoming a therapeutic," he said. "You could potentially enhance the healing of aged tissues by reducing this effect of Wnt signaling on the resident stem cells."
In addition to helping the elderly heal faster and better from muscle injuries, Rando said, the potential benefits could include tissues such as skin, gut and bone marrow, or for that matter, potentially any tissue, such as liver and brain, in which stem cells contribute to normal
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Contact: Louis Bergeron
louisb3@stanford.edu
650-723-3900
Stanford University Medical Center
9-Aug-2007