Age-associated stresses induce an anti-inflammatory senescent phenotype in endothelial cells.
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ABSTRACT: Age is the greatest risk factor for cardiovascular disease. In addition, inflammation and age (senescence) have been linked at both the clinical and molecular levels. In general, senescent cells have been described as pro-inflammatory based on their senescence associated secretory phenotype (SASP). However, we have previously shown that senescence induced by overexpression ofSENEX (or ARHGAP18), in endothelial cells results in an anti-inflammatory phenotype. We have investigated, at the individual cellular level, the senescent phenotype of endothelial cells following three of the chief signals associated with ageing; oxidative stress, disturbed flow and hypoxia. All three stimuli induce senescence and, based on neutrophil adhesion and expression of the adhesion molecules E-selectin and VCA
SUBMITTER: Coleman PR
PROVIDER: S-EPMC3883707 | biostudies-literature | 2013 Dec
REPOSITORIES: biostudies-literature
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