Widespread tissue distribution of steroid sulfatase, 3β-hydroxysteroid dehydrogenase/Δ5-Δ4isomerase(3β-HSD), 17β-HSD5α-reductase and aromatase activities in the rhesus monkey

Martel, Céline; Meiner, Michael H.; Gagné, Donald; Simard, Jacques; Labrie, Fernand

doi:10.1016/0303-7207(94)90056-6

Cited by 181 publications

(100 citation statements)

References 53 publications

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“…The presence of this enzyme in the cardiovascular system has been also documented in previously published reports [1,[6][7][8]. Especially, it has been demonstrated that there were relatively abundant levels of 3b-HSD activity in hearts of experimental animals [7,8]. Expression of 3b-HSD was also reported in human vascular smooth muscle cells (VSMCs) of artery and vein [1,7].…”

supporting

confidence: 52%

“…In addition, the activity of this enzyme is demonstrated not only in classical steroidogenic tissues, but also in many peripheral tissues including human central nervous system [1,[4][5][6]. The presence of this enzyme in the cardiovascular system has been also documented in previously published reports [1,[6][7][8]. Especially, it has been demonstrated that there were relatively abundant levels of 3b-HSD activity in hearts of experimental animals [7,8].…”

mentioning

confidence: 86%

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3β-Hydroxysteroid Dehydrogenase in Human Aorta

et al. 2005

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Abstract. 3b-hydroxysteroid dehydrogenase (3b-HSD) is known to be involved in steroid production and/or metabolism and to be expressed in many tissues including adrenal cortex. Expression of this enzyme has also been elucidated in human cardiovascular system but its details remain largely unknown. Therefore, in this study, we examined the status of 3b-HSD in postmortem human aorta utilizing RT-PCR and immunohistochemical analysis. Both mRNAs and immunoreactivity for the enzyme were detected predominantly in female aorta, and in those with mild atherosclerotic changes. In addition, immunohistochemical study demonstrated that immunoreactivity for 3b-HSD was detected in vascular smooth muscle cells (VSMCs) of aorta. These findings all indicated that steroidogenesis via 3b-HSD may occur in VSMCs of human aorta, possibly related to gender differences and/or the degree of atherosclerosis.

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supporting

confidence: 52%

mentioning

confidence: 86%

3β-Hydroxysteroid Dehydrogenase in Human Aorta

et al. 2005

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“…We hypothesize that the generation of 3βAdiol from testosterone via aromatase-independent pathways, represents a potential mechanism for resistance to AIs. The enzymes required for generation of 3βAdiol, 5α-reductase and 3β-HSD, are both expressed in a wide variety of tissues, primarily the adrenal glands and liver [29]. In addition, we have demonstrated that 3β-HSD is expressed in estrogendeprived breast cancer cells.…”

Section: Discussionmentioning

confidence: 74%

The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: implications for aromatase inhibitor resistance

Sikora

Cordero

Larios

et al. 2008

Breast Cancer Res Treat

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The aromatase inhibitors (AIs) are used to treat estrogen receptor-positive (ER+) breast tumors in post-menopausal women, and function by blocking the conversion of adrenal androgens to estrogens by the enzyme CYP19 aromatase. Breast cancer patients receiving AI therapy have circulating estrogen levels below the level of detection; however, androgen concentrations remain unchanged. We were interested in studying the effects of androgens on breast cancer cell proliferation under profound estrogen-deprived conditions. Using in vitro models of estrogen-dependent breast cancer cell growth we show that the androgens testosterone and 5α-dihydrotestosterone induce the growth of MCF-7, T47D and BT-474 cells in the absence of estrogen. Furthermore, we demonstrate that under profound estrogen-deprived conditions these breast cancer cells up-regulate steroidogenic enzymes that can metabolize androgens to estrogens. Lastly, we found that the downstream metabolite of 5α-dihydrotestosterone, 5α-androstane-3β,17β-diol (3βAdiol), is estrogenic in breast cancer cells, and induces growth and ER-signaling via activation of ERα. In conclusion, our results show that breast cancer cells deprived of estrogen up-regulate steroidogenic enzymes and metabolize androgens to estrogen-like steroids. The generation of estrogen-like steroids represents a potential mechanism of resistance to aromatase inhibitors.

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“…First, fat cells can store and metabolise steroid hormones (17,18). Second, insulin resistance, as is often observed in obesity (19), results in hyperinsulinism and enhanced activity of IGF-I, and has been shown to be associated with increased androgen levels in adolescent girl (20).…”

Section: Introductionmentioning

confidence: 99%

Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche

l’Allemand

Schmidt

Rousson

et al. 2002

European Journal of Endocrinology

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Objective: To explain why adrenal androgens rise with increasing adiposity during childhood, the role of body mass index (BMI), leptin and IGF-I was studied. We also tested whether these parameters contribute to inducing premature adrenarche (PA). Design: In a cross-sectional study, 26 prepubertal obese children were compared with a group of 26 prepubertal children of normal weight, and 30 children under observation for PA were compared with 30 healthy children, matched for gender, bone age and BMI. Methods: Relative contributions of BMI standard deviation scores (SDS) and height SDS, as well as unbound leptin and IGF-I, to the levels of androgens, dehydroepiandrosterone sulfate (DHEAS) and D4-androstenedione (AD) were investigated by means of stepwise regression models. Logarithms of all hormones were standardised for age using residuals of a simple regression analysis, labelled by the suffix ' res '. Results: In the obese children, height SDS, IGF-I res, DHEAS res (all P , 0:05), leptin res ðP , 0:01Þ; and AD res ðP ¼ 0:07Þ were higher than in the controls, and covariates were correlated with each other (leptin res versus BMI SDS r ¼ 0:71; IGF-I res versus height SDS r ¼ 0:61). In the stepwise regression analysis of control and obese children, BMI SDS explained 26% and leptin res explained 12% of the variability of DHEAS res , but this percentage remained at 26% when both variables were simultaneously introduced into the model. In contrast, IGF-I res and BMI SDS alone each accounted for 15% of the variability of AD, and their joint influence accumulated to explain 28% of the variability of AD res . In PA, neither BMI SDS nor leptin res were correlated with the increased androgens. Conclusion: Before the onset of gonadal activity in obese and control children, DHEAS levels, to some extent, are explained by BMI and leptin, while IGF-I in addition to BMI in part accounts for AD levels. Enhanced adrenal androgen secretion in children with PA, however, may be explained by parameters other than leptin or BMI.

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Widespread tissue distribution of steroid sulfatase, 3β-hydroxysteroid dehydrogenase/Δ5-Δ4isomerase(3β-HSD), 17β-HSD5α-reductase and aromatase activities in the rhesus monkey

Cited by 181 publications

References 53 publications

3β-Hydroxysteroid Dehydrogenase in Human Aorta

3β-Hydroxysteroid Dehydrogenase in Human Aorta

The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: implications for aromatase inhibitor resistance

Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche

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Widespread tissue distribution of steroid sulfatase, 3β-hydroxysteroid dehydrogenase/Δ5-Δ4isomerase(3β-HSD), 17β-HSD5α-reductase and aromatase activities in the rhesus monkey

Cited by 181 publications

References 53 publications

3&beta;-Hydroxysteroid Dehydrogenase in Human Aorta

3&beta;-Hydroxysteroid Dehydrogenase in Human Aorta

The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: implications for aromatase inhibitor resistance

Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche

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3β-Hydroxysteroid Dehydrogenase in Human Aorta

3β-Hydroxysteroid Dehydrogenase in Human Aorta