SMAD公司
细胞外基质
辛迪康1
瘢痕疙瘩
信号转导
细胞生物学
MAPK/ERK通路
转化生长因子
Smad2蛋白
化学
细胞外
癌症研究
生物
医学
生物化学
细胞
病理
作者
Jing Cui,Shan Jin,Chenglong Jin,Zhehu Jin
出处
期刊:Life Sciences
[Elsevier]
日期:2020-01-15
卷期号:254: 117326-117326
被引量:22
标识
DOI:10.1016/j.lfs.2020.117326
摘要
The present study aimed to explore the effect of syndecan-1 on keloid fibroblasts.Immunohistochemistry and Western blot were employed to assess the expression of syndecan-1. Primary cultured keloid fibroblasts were transfected with syndecan-1 siRNA. The function of syndecan-1 on the proliferation of keloid fibroblasts was investigated through Cell Counting Kit-8 (CCK-8) and flow cytometry. Extracellular matrix, TGF-β1/Smad, and MAPK related proteins were evaluated by Western blot.Syndecan-1 was significantly overexpressed in both keloid tissues and fibroblasts. Moreover, the knockdown of syndecan-1 remarkably attenuated the proliferation of keloid fibroblasts and reduced the content of the extracellular matrix. Importantly, syndecan-1 regulates the expression of the extracellular matrix in keloid fibroblasts via TGF-β1/Smad and mitogen-activated protein kinase (MAPK) signaling pathways.The current results revealed a crucial function for syndecan-1 in regulating the expression of extracellular matrix and cell proliferation, thereby designating syndecan-1 as a novel target for keloid.
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