Endogenous NO upon estradiol-17β stimulation and NO donor differentially regulate mitochondrial S-nitrosylation in endothelial cells.

ABSTRACT: Adduction of a nitric oxide (NO) moiety (NO(•)) to cysteines termed as S-nitrosylation (SNO) has emerged as a crucial mechanism for NO signaling crucial for mediating the vascular effects of estrogens. Mitochondrion is a known vascular risk factor; however, the effects of estrogens on mitochondrial SNO are incompletely understood. In this study we determined the effects of estradiol-17β (E2β) on mitochondrial protein SNO in primary human umbilical vein endothelial cells and compared the mitochondrial nitroso-proteomes in E2β- and a NO donor S-nitrosoglutathione (GSNO)-treated cells using a proteomics approach. Treatment with 10 nM E2β and 1 mM GSNO for 30 minutes significantly increased the levels of mitochondrial SNO-proteins. Subcellular localization of SNO-proteins showed mitochondria a

SUBMITTER: Satohisa S 

PROVIDER: S-EPMC4098011 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature