DDAH1 deficiency promotes intracellular oxidative stress and cell apoptosis via a miR-21-dependent pathway in mouse embryonic fibroblasts

Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1). Emerging evidence suggests that plasma ADMA accumulation, DDAH1 activity/expression reduction, and microRNA-21 (miR-21) upregulation are linked t...

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Veröffentlicht in:	Free radical biology & medicine 2016-03, Vol.92, p.50-60
Hauptverfasser:	Zhao, Chenyang, Li, Tianhe, Han, Bingxing, Yue, Wenhui, Shi, Linlin, Wang, Hongyun, Guo, Yuting, Lu, Zhongbing
Format:	Artikel
Sprache:	eng
Schlagworte:	ADMA Amidohydrolases - antagonists & inhibitors Amidohydrolases - genetics Amidohydrolases - metabolism Animals Apoptosis - drug effects Arginine - administration & dosage Arginine - analogs & derivatives DDAH1 Embryo, Mammalian - drug effects Embryo, Mammalian - metabolism Endothelial Cells - drug effects Endothelial Cells - metabolism Enzyme Inhibitors - administration & dosage Fibroblasts - drug effects Fibroblasts - metabolism Gene Expression Regulation - drug effects Mice MicroRNAs - genetics MicroRNAs - metabolism miRNA NF-kappa B - genetics Nitric Oxide - genetics Nitric Oxide Synthase Type III - antagonists & inhibitors Nitric Oxide Synthase Type III - genetics Oxidative stress Oxidative Stress - genetics Signal Transduction - drug effects SOD2 Superoxide Dismutase - biosynthesis
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