The decreasion of integrin α5β1/FAK associates with increased apoptosis of aortic smooth muscle cells in acute type A aortic dissection

Author:

Xue Mingming1,Yang Yilin1,Xing Lingyu1,Liao Fengqing1,Xu Feixiang1,Chen Yumei1,Wang Sheng1,Chen Bin1,Yao Chenling1,Gu Guorong1,Tong Chaoyang1,Shao Mian1

Affiliation:

1. Fudan University

Abstract

Abstract Background Acute type A aortic dissection (AAAD) is a devastating condition with the human aortic smooth muscle cells (HASMCs) reduced proliferation and increased apoptosis. Integrin α5β1 and FAK are the important proangiogenic factors involved in regulating angiogenesis. The aim of the study was to investigate the role of integrin α5β1 and FAK in AAAD patients and the potential mechanisms. Methods The aortic tissue samples were collected from 8 AAAD patients and 4 organ donors obtained from Zhongshan Hospital of Fudan University. The level of apoptosis in the aortic tissues were assessed by immunohistochemical staining (ICH) and Terminal-deoxynucleoitidyl transferase mediated nick end labeling assay (TUNEL). The expression of integrin α5β1 and FAK were detected. Furtherly, integrin α5β1 was dificiently expressed in HASMCs and the interaction with FAK was detected by co-immunoprecipitation analysis (Co-IP). The levels of proliferation and apoptosis were assessed by cell-counting Kit-8 analyses (CCK-8) and flow cytometry after integrin α5β1 dificiently. Results The levels of integrin α5β1 and FAK were both significantly decreased in AAAD patients. Down-regulating the expression of integrin α5β1-FAK compound could remarkablely induce the increased apoptosis and decreased proliferation in HASMC, which indicated integrin α5β1-FAK might play a important role in the development of AAAD. Conclusions The down-regulaiton of integrin α5β1-FAK associates with increased apoptosis and decreased proliferation in aortic smooth muscle cells, and might be a potential therapeutic target for AAAD.

Publisher

Research Square Platform LLC

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