Estradiol-Mediated Endothelial Nitric Oxide Synthase Association With Heat Shock Protein 90 Requires Adenosine Monophosphate-Dependent Protein Kinase
Author(s) -
Eberhard Schulz,
Elad Anter,
Ming-Hui Zou,
John F. Keaney
Publication year - 2005
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.105.546812
Subject(s) - medicine , endothelial nitric oxide synthase , heat shock protein , nitric oxide synthase , protein kinase a , adenosine , nitric oxide , endocrinology , shock (circulatory) , microbiology and biotechnology , biochemistry , kinase , enos , biology , gene
Estradiol activates endothelial nitric oxide synthase (eNOS) by mechanisms that involve estrogen receptor-alpha (ERalpha), protein kinase B/Akt, mitogen-activated protein kinases, and heat shock protein 90 (HSP90). Recently, AMP-activated protein kinase (AMPK), an enzyme that plays a crucial role in cellular adaptation to metabolic stress, has been implicated in physiological eNOS activation by the hormones adiponectin and insulin. We therefore investigated whether AMPK is activated by estradiol in endothelial cells and plays a role in estradiol-induced eNOS activation.
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