A decrease in integrin 51/FAK is associated with increased apoptosis of aortic smooth muscle cells in acute type a aortic dissection

Background Acute type A aortic dissection (AAAD) is a devastating disease. Human aortic smooth muscle cells (HASMCs) exhibit decreased proliferation and increased apoptosis, and integrin alpha 5 beta 1 and FAK are important proangiogenic factors involved in regulating angiogenesis. The aim of this study was to investigate the role of integrin alpha 5 beta 1 and FAK in patients with AAAD and the potential underlying mechanisms. Methods Aortic tissue samples were obtained from 8 patients with AAAD and 4 organ donors at Zhongshan Hospital of Fudan University. The level of apoptosis in the aortic tissues was assessed by immunohistochemical (IHC) staining and terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) assays. The expression of integrin alpha 5 beta 1 and FAK was determined. Integrin alpha 5 beta 1 was found to be significantly expressed in HASMCs, and its interaction with FAK was assessed via coimmunoprecipitation (Co-IP) analysis. Proliferation and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assays and flow cytometry after integrin alpha 5 beta 1 deficiency. Results The levels of integrin alpha 5 beta 1 and FAK were both significantly decreased in patients with AAAD. Downregulating the expression of integrin alpha 5 beta 1-FAK strongly increased apoptosis and decreased proliferation in HASMCs, indicating that integrin alpha 5 beta 1-FAK might play an important role in the development of AAAD. Conclusions Downregulation of integrin alpha 5 beta 1-FAK is associated with increased apoptosis and decreased proliferation in aortic smooth muscle cells and may be a potential therapeutic strategy for AAAD.