Estrogen Inhibits Cardiac Hypertrophy: Role of Estrogen Receptor-β to Inhibit Calcineurin (original) (raw)

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2Department of Medicine (A.P., M.V., E.R.L.), University of California, Irvine, Irvine, California 92697

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1Department of Medicine (M.R., E.R.L.), Veteran’s Affairs Medical Center Long Beach, Long Beach, California 90822

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3Department of Biochemistry (D.L., J.L.), University of Missouri, Columbia, Missouri 65211

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3Department of Biochemistry (D.L., J.L.), University of Missouri, Columbia, Missouri 65211

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2Department of Medicine (A.P., M.V., E.R.L.), University of California, Irvine, Irvine, California 92697

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1Department of Medicine (M.R., E.R.L.), Veteran’s Affairs Medical Center Long Beach, Long Beach, California 90822

2Department of Medicine (A.P., M.V., E.R.L.), University of California, Irvine, Irvine, California 92697

*Address all correspondence and requests for reprints to: Ellis R. Levin M.D., Medical Service (111-I), Long Beach Veteran’s Affairs Medical Center/University of California-Irvine, 5901 East 7th Street, Long Beach, California 90822.

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28 January 2008

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Ali Pedram, Mahnaz Razandi, Dennis Lubahn, Jinghua Liu, Mani Vannan, Ellis R. Levin, Estrogen Inhibits Cardiac Hypertrophy: Role of Estrogen Receptor-β to Inhibit Calcineurin, Endocrinology, Volume 149, Issue 7, 1 July 2008, Pages 3361–3369, https://doi.org/10.1210/en.2008-0133
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Estrogen has been reported to prevent development of cardiac hypertrophy in female rodent models and in humans. However, the mechanisms of sex steroid action are incompletely understood. We determined the cellular effects by which 17β-estradiol (E2) inhibits angiotensin II (AngII)-induced cardiac hypertrophy in vivo. Two weeks of angiotensin infusion in female mice resulted in marked hypertrophy of the left ventricle, exacerbated by the loss of ovarian steroid hormones from oophorectomy. Hypertrophy was 51% reversed by the administration of E2 (insertion of 0.1 mg/21-d-release tablets). The effects of E2 were mainly mediated by the estrogen receptor (ER) β-isoform, because E2 had little effect in ERβ-null mice but comparably inhibited AngII-induced hypertrophy in wild-type or ERα-null mice. AngII induced a switch of myosin heavy chain production from α to β, but this was inhibited by E2 via ERβ. AngII-induced ERK activation was also inhibited by E2 through the β-receptor. E2 stimulated brain natriuretic peptide protein expression and substantially prevented ventricular interstitial cardiac fibrosis (collagen deposition) as induced by AngII. Importantly, E2 inhibited calcineurin activity that was stimulated by AngII, related to E2 stimulating the modulatory calcineurin-interacting protein (MCIP) 1 gene and protein expression. E2 acting mainly through ERβ mitigates the important signaling by AngII that produces cardiac hypertrophy and fibrosis in female mice.

Copyright © 2008 by the Endocrine Society

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