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• W2024883268 endingPage "2034" @default.
• W2024883268 startingPage "2027" @default.
• W2024883268 abstract "Oxidative stress (OS) induces smooth muscle cell apoptosis in the atherosclerotic plaque, leading to plaque instability and rupture. Heme oxygenase-1 (HO-1) exerts cytoprotective effects in the vessel wall. Recent evidence suggests that PKB/Akt may modulate HO-1 activity. This study examined the role of Akt in mediating the cytoprotective effects of HO-1 in OS-induced apoptosis of human aortic smooth muscle cells (HASMCs).HASMCs were transduced with retroviral vectors expressing HO-1, Akt, or GFP and exposed to H2O2. Cell viability was assessed by MTT assay. OS was determined by CM-H2DCFDA fluorescence, and apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), caspase-3 activity, and Bcl-2/Bad levels. Mitochondrial membrane potential (delta psi(m)) was assessed by fluorescence-activated cell sorter (FACS) using JC-1. HO-1 reduced H2O2-induced OS and apoptosis. Akt knockdown removed the protective effect of HO-1 on delta psi(m) during exposure to H2O2. Conversely, HO-1 knockdown removed the protective effect of Akt on delta psi(m). Inhibition of PI3K-Akt reduced induction of HO-1 protein expression by H2O2 and blocked its anti-apoptotic effects. The Akt-mediated upregulation of HO-1 was dependent on activation of HO-1 promoter by Nrf2.HO-1 and Akt exert codependent cytoprotective effects against OS-induced apoptosis in HASMCs. These findings may have implications for the design of novel therapeutic strategies for plaque stabilization." @default.
• W2024883268 created "2016-06-24" @default.
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• W2024883268 date "2006-09-01" @default.
• W2024883268 modified "2023-09-30" @default.
• W2024883268 title "Protection of Human Vascular Smooth Muscle Cells From H ₂ O ₂ -Induced Apoptosis Through Functional Codependence Between HO-1 and AKT" @default.
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• W2024883268 doi "https://doi.org/10.1161/01.atv.0000236204.37119.8d" @default.
• W2024883268 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16840713" @default.
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