Key result
Asymmetric dimethylarginine induces endothelial nitric-oxide synthase redistribution to the mitochondria through nitration-mediated activation of Akt1 at Tyr350.
Population
Ovine pulmonary artery endothelial cells (PAEC), COS-7 cells, and HEK 293 cells
Comparison
Exposure to asymmetric dimethylarginine or… vs Vehicle control or untreated cells
Design
Preclinical
Authors
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No immediate clinical application; extends mechanistic understanding of ADMA effects on eNOS.
p-value: p=<0.05
ADMA induces eNOS translocation to mitochondria via Akt1 nitration at Tyr350 and subsequent phosphorylation of eNOS, revealing a novel mechanism of endothelial regulation.
Rafikov et al. (2012) studied Endothelial dysfunction (in vitro model). Asymmetric dimethylarginine (ADMA) vs. Vehicle control was evaluated on eNOS mitochondrial translocation and Akt1 activation (p=<0.05). Asymmetric dimethylarginine induces endothelial nitric-oxide synthase redistribution to the mitochondria through nitration-mediated activation of Akt1 at Tyr350.
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