17beta-Estradiol induces protein S-nitrosylation in the endothelium

Cardiovascular Research
Subhadeep ChakrabartiSandra T Davidge

Abstract

Estrogen induces nitric oxide (NO) in the endothelium and appears to protect against inflammation and atherosclerosis. NO can induce post-translational protein modifications such as cysteine S-nitrosylation in the cellular proteins which may exert anti-inflammatory effects. However, whether estrogen can induce protein S-nitrosylation in the endothelium is not known. Given this background, we investigated the role of 17beta-estradiol (E2beta), the major form of estrogen in the body, on endothelial protein S-nitrosylation. Experiments were performed in human umbilical vein endothelial cells (HUVECs). S-nitrosylation was detected by immunostaining for nitrosocysteine and further confirmed by biotin switch method. Ovariectomized 12-month-old Sprague-Dawley rats with/without estradiol supplementation were used for in vivo validation of findings. We found that physiologically relevant doses of E2beta increased protein S-nitrosylation in HUVECs through estrogen receptor-alpha (ERalpha) and endothelial nitric oxide synthase (eNOS). Interestingly, specific agonists for both ERalpha and ERbeta increased eNOS protein expression, while only the former could activate eNOS through phosphorylation. S-nitrosylation by E2beta prevented angioten...Continue Reading

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