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Angiotensin II induces endothelial cell senescence via the activation of mitogen‐activated protein kinases
Author(s) -
Shan HaiYan,
Bai XiaoJuan,
Chen XiangMei
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1467
Subject(s) - senescence , microbiology and biotechnology , mapk/erk pathway , angiotensin ii , kinase , signal transduction , biology , protein kinase a , mitogen activated protein kinase , cell growth , biochemistry , receptor
Vascular endothelial cells have a finite cell lifespan and eventually enter an irreversible growth arrest, cellular senescence. The functional changes associated with cellular senescence are thought to contribute to human aging and age‐related cardiovascular disorders, for example, atherosclerosis. Angiotensin II (Ang II), a principal effector of the renin‐angiotensin system (RAS), an important signaling molecule involved in atherogenic stimuli, is known to promote aging and cellular senescence. In the present study, induction of Ang II promoted a growth arrest with phenotypic characteristics of cell senescence, such as enlarged cell shapes, increased senescence‐associated ß‐galactosidase (SA‐ß‐gal) positive staining cells, and depressed cell proliferation. Ang II drastically decreased the expression level of Bcl‐2, in part via the activation of extracellular signal‐regulated kinase (ERK). Our results suggest that Ang II can induce HUVEC senescence; one of its molecular mechanisms is a probability that the mitogen‐activated protein kinase (MAPK) signal pathway is involved in the process of pathological and physiological senescence of endothelial cells as well as vascular aging. Copyright © 2008 John Wiley & Sons, Ltd.