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From autophagy to senescence and apoptosis in Angiotensin II ‐treated vascular endothelial cells
Author(s) -
Shan Haiyan,
Guo Dawei,
Li Xuelian,
Zhao Xin,
Li Wan,
Bai Xiaojuan
Publication year - 2014
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12242
Subject(s) - autophagy , apoptosis , senescence , microbiology and biotechnology , angiotensin ii , atg5 , endothelial stem cell , chemistry , flow cytometry , cell , biology , biochemistry , receptor , in vitro
The aim of this study was to explore if cell autophagy is activated by Ang II before aging using human umbilical vascular endothelial cells ( HUVEC s). The ultrastructural analysis of HUVEC s was performed to observe autophagosomes. The LC 3‐ II / LC 3‐I ratio was determined by western blot assay. The β‐gal staining was used to identify cell senescence. The flow cytometry was performed to evaluate cell apoptosis. The BH 3 domain analog ABT 737 or Beclin‐1 knockdown by specific sh RNA or valsartan was applied to investigate their effects on cell autophagy, senescence, and apoptosis induced by Ang II . Cell autophagy was initiated after Ang II treatment at 24 h. And cell senescence and apoptosis were observed in Ang II ‐treated cells at 48 h. The significant interaction of Beclin‐1 and Bcl‐2 was detected at 48 h after Ang II treatment. Beclin‐1 was indispensable to Ang II ‐induced autophagy, and its BH 3 domain was required for the interaction with Bcl‐2 to attenuate autophagy. Pretreated with valsartan, cells were present with less autophagic, senescent, and apoptotic cells after Ang II stimulation. In conclusion, Ang II induced autophagy, senescence, and apoptosis of HUVEC s progressively, and autophagy presented an early protective effect on vascular endothelial damage due to Ang II .