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dc.contributorVirginia Tech
dc.contributor.authorLiu, D. M.
dc.contributor.authorJiang, H. L.
dc.contributor.authorGrange, R. W.
dc.date.accessioned2014-07-08T13:02:18Z
dc.date.available2014-07-08T13:02:18Z
dc.date.issued2005-03
dc.identifier.citationDongmin Liu, Honglin Jiang, and Robert W. Grange. "Genistein Activates the 3′,5′-Cyclic Adenosine Monophosphate Signaling Pathway in Vascular Endothelial Cells and Protects Endothelial Barrier Function," Endocrinology 2005 146:3, 1312-1320. DOI: http://dx.doi.org/10.1210/en.2004-1221
dc.identifier.issn0013-7227
dc.identifier.urihttp://hdl.handle.net/10919/49393
dc.description.abstractThe soy phytoestrogen, genistein, has an array of biological actions, including weak estrogenic effects, inhibition of tyrosine kinase, and cellular antioxidant activity. Recent studies showed that genistein may improve vascular function, but the mechanism is unclear. We show that genistein stimulates intracellular cAMP accumulation in intact bovine aortic endothelial cells and human umbilical vein endothelial cells over an incubation period of 30 min. Increases in intracellular cAMP are evoked by as low as 10 nM genistein but not by estrogen. These increases in cAMP may result primarily from enhanced adenylate cyclase activity by a mechanism that does not involve genomic actions or estrogen receptors. The cAMP induced by genistein activates cAMP-dependent protein kinase (PKA) in bovine aortic endothelial cells. The activation of PKA phosphorylates and activates cAMP response element binding protein, leading to up-regulation of cAMP response element-containing gene expression. In addition, activation of PKA protects thrombin-induced endothelial monolayer permeability, a novel cardioprotective effect of genistein mediated by the cAMP/PKA cascade. These findings demonstrate that a nongenomic action of genistein leads to activation of the cAMP/PKA signaling system to protect the vascular barrier function and alter the expression of cAMP-regulated genes, thereby providing a novel mechanism underlying some of the cardiovascular protective effects proposed for soy phytoestrogens.
dc.description.sponsorshipSupport Program Innovative Research Strategies Seed Grant from Virginia Polytechnic Institute and State University
dc.language.isoen_US
dc.publisherEndocrine Society
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectestrogen-receptor-alpha
dc.subjectnitric-oxide synthase
dc.subjectstress stimulates
dc.subjectphosphorylation
dc.subjecttyrosine kinase inhibitor
dc.subjectcyclic-amp accumulation
dc.subjectsmooth-muscle-cells
dc.subjectsoy isoflavones
dc.subjectpostmenopausal women
dc.subjectgrowth-factor
dc.subjectphytoestrogen genistein
dc.subjectendocrinology & metabolism
dc.titleGenistein activates the 3 ',5 '-cyclic adenosine monophosphate signaling pathway in vascular endothelial cells and protects endothelial barrier function
dc.typeArticle - Refereed
dc.contributor.departmentAnimal and Poultry Sciencesen_US
dc.contributor.departmentHuman Nutrition, Foods, and Exerciseen_US
dc.identifier.urlhttp://press.endocrine.org/doi/abs/10.1210/en.2004-1221
dc.date.accessed2014-07-07
dc.title.serialEndocrinology
dc.identifier.doihttps://doi.org/10.1210/en.2004-1221


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