Necrostatin-1, RIP1/RIP3 inhibitor, relieves transforming growth factor β-induced wound-healing process in formation of hypertrophic scars

被引：7
|
作者：
Lin, Pei-Ting [1 ]
Xue, Xiao-Dong [1 ]
Zhao, Zhong-Dong [1 ]
Lu, Jun-Yang [1 ]
Xie, Pei-Lin [1 ]
机构：
[1] Gansu Prov Hosp, Dept Plast Surg, 204 Donggang West Rd, Lanzhou 73000, Gansu, Peoples R China
来源：
JOURNAL OF COSMETIC DERMATOLOGY | 2021年 / 20卷 / 08期
关键词：
hypertrophic scars; necrostatin‐ 1; receptor‐ interacting protein kinase; transforming growth factor β wound healing; MATRIX;
D O I：
10.1111/jocd.13860
中图分类号：
R75 [皮肤病学与性病学];
学科分类号：
100206 ;
摘要：
Background Hypertrophic scars (HS) are common pathologic processes emerged during wound-healing process. The receptor-interacting protein kinase (RIP) might participate in keloid formation. Aims This study aimed to investigate Necrostatin-1 (Nec-1), a RIP1/RIP3 inhibitor, in the formation of hypertrophic scar. Methods Human hypertrophic scar fibroblasts (HSF) were extracted from patients with hypertrophic scar. Transforming growth factor-beta 1 (TGF-beta 1) was performed to induce wound-healing process including cell proliferation (CCK-8, Flow cytometry, and Western blot), migration (Transwell assay, Western blot), collagen production (Western blot), and extracellular matrix dysfunction (Western blotting and immunofluorescence). Results Our results reported that Nec-1 inhibited TGF-beta 1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-beta 1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-beta 1-induced HSF. Besides, Nec-1 also reduced TGF-beta 1-induced collagen production and alpha-smooth muscle actin expression in HSF. Conclusions The present data in this study showed the potential role of Nec-1 as a novel treatment for HS.
引用
收藏
页码：2612 / 2618
页数：7
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