Abstract
Background: Genistein (GST) is a phytoestrogen that binds estrogen receptors (ER) to produce a protective cardiovascular effect. It also has been shown binding peroxisome proliferator-activated receptor-γ (PPAR-γ). Methods: In the present study, we assessed the role of PPAR-γ and ER in GST-mediated regulation of vascular tone in female rat aortas by in vitro tension measurement, immunohistochemistry, immunofluorescence, immunoprecipitation and Western blot analysis. Results: In aortas pretreated with GW9662 (inhibitor of PPAR-γ), ICI182780 (inhibitor of ER) and a combination of GW9662 and ICI182780, the magnitudes of GST-induced dilatation were attenuated. N(G)-nitro-L-arginine methyl ester had a similar effect. ER-β and PPAR-γ colocalized in all 3 layers of the aortas, while ER-α and PPAR-γ colocalized only in the vascular endothelium and adventitia. In GST-treated whole-cell protein samples, we demonstrated coimmunoprecipitation of ER-β (not ER-α) and PPAR-γ. The expression of ER-β and PPAR-γ in nuclear protein from GST-treated samples increased, which was partially reversed by either GW9662 or ICI182780 and more efficiently reversed using a combination of GW9662 and ICI182780. Conclusion: Our findings suggest that GST can relax phenylephrine-induced vascular contraction in female rat aortas, which is mediated by PPAR-γ and ER-β.
Published Version
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