Double-Stranded RNA Activates Toll-Like Receptor 3 (TLR3) to Promote Regeneration of Skin and Hair Follicles During Wound Healing; Drugs to Turn On TLR3 Might Further Promote Tissue Regeneration in Patients Scarred from Injury, Hopkins Study Suggests

Johns Hopkins researchers have identified a novel cell signaling pathway in mice, through which mammals, presumably including humans, can regenerate hair follicles and skin while healing from wounds. The discovery, summarized in a featured, open-access article published online on August 6, 2015 in the journal Cell Stem Cell, could, the scientists say, eventually help spur the growth of new hair, skin, or other organ tissue in scarred victims of burns and other injuries. The article is titled “dsRNA Released by Tissue Damage Activates TLR3 to Drive Skin Regeneration.” The study "uncovers a novel role for a protein [TLR3] that works as a master regulator of regeneration in the skin," says senior study author Luis A. Garza, M.D., Ph.D., Associate Professor of Dermatology at the Johns Hopkins University School of Medicine. "Medications that turn on this protein have the powerful potential to decrease scarring as healing of wounds takes place, thereby promoting skin and hair follicle regeneration." Dr. Garza says his team's work is based on the knowledge that damaged skin releases double-stranded RNA (dsRNA) -- genetic information normally carried by some viruses -- that is sensed by a protein called toll-like receptor 3 (TLR3) (image illustrates structure of TLR3 protein). TLR3, which in other contexts plays a fundamental role in recognizing some disease-causing organisms and activating the immune system, also, in response to wounding activates the genes IL6 and STAT3 to promote hair follicle regeneration.
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