CLC-3 regulates TGF-β/smad signaling pathway to inhibit the process of fibrosis in hypertrophic scar

Objective: To study the role and mechanism of chloride channel-3 (ClC-3) in the formation of hypertrophic scar by constructing ClC-3 interference vectors and examining their effects on human hypertrophic scar fibroblasts (HSFB). Methods: Human HSFB and human normal skin fibroblasts (NSFB) were used in this study, and ClC-3 interference vectors were constructed to transfect cells. ClC-3 inhibitors NPPB and Tamoxifen were used to treat cells. Cell migration and the expression of TGF-beta/Smad, CollagenI, CollagenIII were examined to explore the role of ClC-3 in the formation of hypertrophic scar. Results: Compared with the normal skin tissue, the positive expression of ClC-3 and TGF-beta in the scar tissue was significantly increased. The relative expression of ClC-3 and TGF-beta 1 in HSFB cells was higher than that in NSFB cells. Interfering with the expression of CLC-3 can inhibit the migration of HSFB cells and the expression of TGF- beta/Smad, CollagenI/III. The experiment of HSFB cells treated by CLC-3 inhibitors can also obtain similar results. Conclusion: Inhibiting CLC-3 can reduce the formation of hypertrophic scars.