Notch信号通路
活力测定
细胞内
增生性瘢痕
医学
槽口1
细胞凋亡
小干扰RNA
流式细胞术
细胞生物学
真皮
发病机制
分子生物学
信号转导
病理
细胞
癌症研究
细胞生长
细胞培养
生物
免疫学
转染
生物化学
遗传学
作者
Lin Chen,Xi Zhang,Zhou Yu,Yajuan Song,Tong Wang,Kuan Yang,Shengxu Li,Jianzhang Wang,Yingjun Su,Bao-qiang Song
出处
期刊:Annals of Plastic Surgery
[Ovid Technologies (Wolters Kluwer)]
日期:2020-09-01
卷期号:86 (4): 400-405
被引量:2
标识
DOI:10.1097/sap.0000000000002540
摘要
Background Hypertrophic scar (HS) is the most common complication after skin injury with unknown etiopathogenesis. There is increasing evidence to suggest that aberrant Notch signaling contributes directly to skin pathogenesis and altered expression of the Notch intracellular domain (NICD) identified in HS. Therefore, the aim of this study was to investigate the effects of Notch signaling pathway in HS pathogenesis. Methods Hypertrophic scar and normal skin samples were collected. Notch intracellular domain expression was detected by immunohistochemistry staining and fibroblasts were separated from the samples. We compared fibrotic factors production, cell viability, migration and apoptosis of HS fibroblasts (HFB) versus normal skin fibroblasts (NFB) by real time quantitative polymerase chain reaction, MTS, cell scratch assay and flow cytometry respectively under the impact of inhibition of Notch signaling by NICD-small-interfering RNA (SiRNA). Results The results showed that NICD was overexpressed in the dermis of HS tissues. Inhibition of Notch signaling by NICD-SiRNA suppressed the production of the fibrotic factors including collagen 1, collagen 3, α-SMA, and TGF-β1 by HFB and NFB. Cell viability and migration were reduced in NICD-SiRNA–treated NFB and HFB, whereas cell apoptosis was enhanced by NICD-SiRNA. Conclusions Conclusively, the study demonstrates a potential role for Notch signaling in HS progression, and targeting this pathway may provide a novel strategy for treatment of HS.
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