CLC-3 Regulates TGF-β/smad Signaling Pathway to Inhibit the Process of Fibrosis in Hypertrophic Scar

Overview

Journal Heliyon

Specialty Social Sciences

Date 2024 Feb 9

PMID 38333829

Authors

Qian Liang

Fuqiang Pan

HouHuang Qiu

Xiang Zhou

Jieyun Cai

Ruijin Luo

Zenghui Xiong

Huawei Yang

Liming Zhang

Affiliations

Soon will be listed here.

Abstract

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-β/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-β in the scar tissue was significantly increased. The relative expression of ClC-3 and TGF-β1 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- β/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.

Citing Articles

HOXC10 promotes hypertrophic scar fibroblast fibrosis through the regulation of STMN2 and the TGF-β/Smad signaling pathway.

Zhou X, Lin S Histochem Cell Biol. 2024; 162(5):403-413.

PMID: 39152325 DOI: 10.1007/s00418-024-02317-6.

Isorhamnetin inhibits hypertrophic scar formation through TGF-β1/Smad and TGF-β1/CREB3L1 signaling pathways.

Wu J, Song Y, Wang J, Wang T, Yang L, Shi Y Heliyon. 2024; 10(13):e33802.

PMID: 39055792 PMC: 11269880. DOI: 10.1016/j.heliyon.2024.e33802.

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