The experiment shows that β1-integrin – one of 28 types of integrin – maintains a link between the stem cell and its environment, and interacts biochemically with a growth factor called fibroblast growth factor [FGF] to promote stem cell growth and restoration after muscle tissue injury. Aged stem cells do not respond to FGF, and the results also show that β1-integrin restores aged stem cell’s ability to respond to FGF to grow and improve muscle regeneration.
By tracking an array of proteins inside the stem cells, the researchers tested the effects of removing β1-integrin from the stem cell. This is based on the understanding that the activities of stem cells are dependent on their environment and supported by the proteins found there. “If we take out β1-integrin, all these other (proteins) are gone,” said Fan, Carnegie Institution for Science in Washington and Baltimore. Why that is the case is not clear, but the experiment showed that without β1-integrin, stem cells could not sustain growth after muscle tissue injury.
By examining β1-integrin molecules and the array of proteins that they used to track stem cell activity in aged muscles, they found that all of these proteins looked like they had been removed from aged stem cells. They injected an antibody to boost β1-integrin function into aged muscles to test whether this treatment would enhance muscle regeneration. Measurements of muscle fiber growth with and without boosting the function of β1-integrin showed that the protein led to as much as 50% more regeneration in cases of injury in aged mice.
When the same β1-integrin function-boosting strategy was applied to mice with muscular dystrophy, the muscle was able to increase strength by about 35%.
They will next try to determine what is happening inside the stem cells as they react with their immediate environment to understand more about the interaction of the two. That, in turn, could help refine the application of integrin as a therapy for muscular dystrophy and other diseases, and for age-related muscle degeneration. “We provide here a proof-of-principle study that may be broadly applicable to muscle diseases that involve SC (stem cell) niche dysfunction,” the authors wrote. “But further refinement is needed for this method to become a viable treatment.” http://releases.jhu.edu/2016/07/19/protein-found-to-bolster-growth-of-damaged-muscle-tissue/
http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.4116.html
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