SIRT1 inhibits TGF--induced endothelial-mesenchymal transition in human endothelial cells with Smad4 deacetylation

被引：33
|
作者：
Li, Zhen [1 ]
Wang, Fei [1 ]
Zha, Siyuan [1 ]
Cao, Qing [1 ]
Sheng, Jing [2 ]
Chen, Shuyan [1 ]
机构：
[1] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Geriatr, 1665 Kong Jiang Rd, Shanghai 200092, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Geriatr, Shanghai, Peoples R China
来源：
JOURNAL OF CELLULAR PHYSIOLOGY | 2018年 / 233卷 / 11期
基金：
中国国家自然科学基金;
关键词：
endothelial-mesenchymal transition (EndMT); fibrosis; SIRT1; Smad4; TGF-beta; CARDIAC FIBROSIS; IN-VITRO; CONTRIBUTES; TGF-BETA/SMAD3; METASTASIS; APOPTOSIS; RESPONSES; PROTECTS; PATHWAY; VIVO;
D O I：
10.1002/jcp.26846
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Endothelial-mesenchymal transition (EndMT) plays a pivotal role in organ fibrosis. This study examined the effect of SIRT1 on transforming growth factor beta (TGF-)-induced EndMT in human endothelial cells (ECs) and its probable molecular mechanism. We assessed EndMT by immunofluorescence staining, quantitative real-time polymerase chain reaction, Western blotting, and migration and invasion assays. Adenovirus was used to overexpress or knockdown SIRT1 in ECs. The regulatory relationship between SIRT1 and Smad4 was analyzed by coimmunoprecipitation assay. We found that SIRT1 was decreased in TGF--induced EndMT, and SIRT1 inhibited TGF--induced EndMT through deacetylating Smad4. Our findings suggest that SIRT1 has an important role in inhibiting EndMT by regulating the TGF-/Smad4 pathway in human ECs and, thus, protecting against fibrosis.
引用
收藏
页码：9007 / 9014
页数：8
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