Sexual dimorphism characterizes baboon myocardial androgen receptors but not myocardial estrogen and progesterone receptors

Lin, Alan; Schultz, James J.; Brenner, Robert; Shain, Sydney A.

doi:10.1016/0960-0760(90)90376-v

Cited by 25 publications

(12 citation statements)

References 44 publications

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“…17 We found sex differences in ER-␤ expression in controls and a 2.5-fold greater ER-␤ increase with aortic stenosis in female hearts. From the statistical point of view, our sample size was only moderate.…”

Section: Discussionmentioning

confidence: 75%

Upregulation of Myocardial Estrogen Receptors in Human Aortic Stenosis

et al. 2004

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Background-Estrogen receptor (ER)-mediated effects have been associated with the modulation of myocardial hypertrophy in animal models and in humans, but ER expression in the human heart and its relation to hypertrophymediated gene expression have not yet been analyzed. We therefore investigated sex-and disease-dependent alterations of myocardial ER expression in human aortic stenosis together with the expression of hypertrophy-related genes. Methods and Results-ER-␣ and -␤, calcineurin A-␤, and brain natriuretic peptide (BNP) mRNA were quantified by real-time polymerase chain reaction in left ventricular biopsies from patients with aortic valve stenosis (nϭ14) and control hearts with normal systolic function (nϭ17). ER protein was quantified by immunoblotting and visualized by immunofluorescence confocal microscopy. ER-␣ mRNA and protein were increased 2.6-fold (Pϭ0.003) and 1.7-fold (Pϭ0.026), respectively, in patients with aortic valve stenosis. Left ventricular ER-␤ mRNA was increased 2.6-fold in patients with aortic valve stenosis (PϽ0.0001). ER-␣ and -␤ were found in the cytoplasm and nuclei of human hearts. A strong inverse correlation exists between ER-␤ and calcineurin A-␤ mRNA in patients with aortic valve stenosis (rϭϪ0.83, Pϭ0.002) but not between ER-␣ or -␤ and BNP mRNA. Conclusions-ER-␣ and -␤ in the human heart are upregulated by myocardial pressure load.

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Section: Discussionmentioning

confidence: 75%

Upregulation of Myocardial Estrogen Receptors in Human Aortic Stenosis

et al. 2004

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“…The present study and preceding studies make it likely that the important effectors are androgens, not estrogen, because estrogen receptors have been detected in the atria but have been difficult to unequivocally demonstrate in ventricular myocytes. 21,46 Moreover, changes in cardiac electrophysiological properties correspond temporally to changes in the androgen but not estrogen milieu (see below).…”

Section: Discussionmentioning

confidence: 99%

“…19 To date, there has been no unequivocal evidence that androgens can produce a hypertrophic effect directly on cardiac myocytes independent of other neurohormonal or hemodynamic effects that alter preload and/or afterload, although there is immunohistochemical evidence that androgen receptors are present in some cell types within the myocardium. 20,21 Therefore, we undertook the present study to determine whether in adult mammalian heart, and specifically in cardiac myocytes, androgen receptors are present in a molecular context that permits regulation of cardiac hypertrophy by exogenous androgens. We now report that the androgen receptor gene is expressed specifically in cardiac myocytes and that androgens can mediate a significant hypertrophic response directly in cardiac myocytes.…”

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confidence: 99%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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Background-The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain.Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. Methods and Results-We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [ 3 H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. Conclusions-Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.(Circulation. 1998;98:256-261.)

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“…The findings of the present study demonstrate for the first time that exposure to physiological concentrations of gonadal steroids (Scott et al, 1980a,b;Lou et al, 1986) and C (Sower and Schreck, 1982) can promote myocardial contractility in rainbow trout. From studies on mammals, it is also becoming increasingly clear that sex-specific differences exist in hormone signaling and the cardiovascular system (Lin et al, 1990;Beyer et al, 2001). Our data indicate that T, 11KT and C promote positive inotropism in hearts from sexually immature or mature male trout, whereas hearts from immature females only respond to E2 and C. The observation of sex-dependent responsiveness to steroids in the fish heart is consistent in most cases with the presence of particular hormones in the blood, with T being an exception.…”

Section: Discussionmentioning

confidence: 99%

Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout

Farrar

Rodnick

2004

Journal of Experimental Biology

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The purpose of this study was to determine whether steroid hormones modulate cardiac function in rainbow trout (Oncorhynchus mykiss Walbaum). We assessed the effects of exogenously administered steroids on isolated ventricle strips and report that physiological concentrations of androgens, 17β-estradiol and cortisol rapidly (<10·min) enhance inotropism (30-40%) in a sexspecific manner. These effects were specific to the hormones studied, absent if animals were anesthetized chemically and dependent upon steroid concentration and contraction frequency. Based on the use of specific steroid receptor antagonists and key enzyme inhibitors, it appears that testosterone, 11-ketotestosterone and cortisol each act through specific intracellular receptors in males and that the positive inotropism requires the synthesis of polyamines and nitric oxide. Cortisol and 17β-estradiol, but not androgens, had similar effects in females and also involved similar signaling pathways. Androgen and cortisol effects were additive in males but cortisol and 17β-estradiol were not additive in females, suggesting sex differences in the pathways through which these hormones stimulate inotropism. In summary, gonadal steroids and cortisol promote ventricular contractility in a sexdependent manner through mechanisms that appear multifaceted. Ultimately, steroid-mediated improvements in cardiac performance might involve non-genomic pathways and be physiologically important during migration, spawning or stressful periods.

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Sexual dimorphism characterizes baboon myocardial androgen receptors but not myocardial estrogen and progesterone receptors

Cited by 25 publications

References 44 publications

Upregulation of Myocardial Estrogen Receptors in Human Aortic Stenosis

Upregulation of Myocardial Estrogen Receptors in Human Aortic Stenosis

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout

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