Title: Role of TRPC3 in wound contraction / Papers of The 9th Japan Scar Workshop


Papers of The 9th Japan Scar Workshop
1. Title: Role of TRPC3 in wound contraction Authors: Kenichiro Kawai, Hisako Ishise, Toshihiro Fujiwara, Soh Nishimoto, and Masao Kakibuchi Affiliation: Department of Plastic Surgery, Hyogo College of Medicine
Purpose: Mechanical force is thought to have some effects on the wound healing process, especially in the formation of hypertrophic scar contractures. Here, we investigated the role that TRPC3 plays in wound contraction as a mechanotransducer. Methods: TRPC3-overexpressing NIH3T3 mouse fibroblasts were created using a PMXS-IRES-GFP system. TRPC3-overexpressing fibroblasts or vector-transfected control fibroblasts were embedded in type I collagen. Then, the TRPC agonist Endothelin1, the Endothelin1 antagonist PD142893, or the TRPC3 blocker Pyr3 was added and the contraction rates of the gels were analyzed. Next, these fibroblasts or the same amount of normal saline were injected into the entire dorsal area of 8-week-old female Balb/c nu/nu mice. At 7 days post-transplantation, bilateral dorsal cutaneous wounds were created and the rate of wound closure was measured. Results: Gels containing TRPC3-overexpressing fibroblasts contracted more than control gels. Moreover, adding Endothelin1 to the gels increased the contractile activity, which was attenuated by PD142893. Transplantation of TRPC3-overexpressing fibroblasts resulted in a statistically significant increase in wound contraction at all time points. Conclusions: The TRPC3 channel is a potential mechanical force transducer that plays an important role in the pathogenesis of hypertrophic scar contracture.
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