Gastric estradiol-17β (E2) and liver ERα correlate with serum E2 in the cholestatic male rat

Kobayashi, Hiroto; Yoshida, Saori; Sun, Yingjie; Shirasawa, Nobuyuki; Naito, Akira

doi:10.1530/joe-13-0156

Cited by 19 publications

(12 citation statements)

References 34 publications

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“…It is known that in mammals, including humans, aromatase is expressed in peripheral organs/tissues such as bones, skin, adrenals and adipose tissue (Conley and Hinshelwood, 2001; Czajka-Oraniec and Simpson, 2010; Moreau et al, 2009; Simpson, 2004; Simpson et al, 2001). Aromatase expression and estrogen production have also been reported in the stomach of female rats (Kobayashi et al, 2013, 2015) as well as AA in the quail liver (Silverin et al, 2000). In zebra finches, one study compared AA in different tissues and concluded that the brain, besides the ovary, seems to be the only site of estrogen synthesis since AA was undetected in the adrenals, muscle, skin, liver, adipose tissue, kidney, and heart (Schlinger and Arnold, 1991).…”

Section: Discussionmentioning

confidence: 94%

Non-ovarian aromatization is required to activate female sexual motivation in testosterone-treated ovariectomized quail

Bournonville

Balthazart

Ball

et al. 2016

Hormones and Behavior

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Although aromatase is expressed in both male and female brains, its functional significance in females remains poorly understood. In female quail, sexual receptivity is activated by estrogens. However it is not known whether sexual motivation is similarly estrogen-dependent and whether estrogens locally produced in the brain contribute to these behavioral responses. Four main experiments were designed to address these questions. In experiment 1 chronic treatment of females with the anti-estrogen tamoxifen decreased their receptivity, confirming that this response is under the control of estrogens. In experiment 2 chronic treatment with tamoxifen significantly decreased sexual motivation as treated females no longer approached a sexual partner. In experiment 3 (a) ovariectomy (OVX) induced a significant decrease of time spent near the male and a significantly decreased receptivity compared to gonadally intact females, (b) treatment with testosterone (OVX+T) partially restored these responses and (c) this effect of T was prevented when estradiol synthesis was inhibited by the potent aromatase inhibitor Vorozole (OVX+T+VOR). Serum estradiol concentration was significantly higher in OVX+T than in OVX or OVX+T+VOR females. Together these data demonstrate that treatment of OVX females with T increases sexual motivation and that these effects are mediated at least in part by non-gonadal aromatization of the androgen. Finally, assays of aromatase activity on brain and peripheral tissues (Experiment 4) strongly suggest that brain aromatization contributes to behavioral effects observed here following T treatment but alternative sources of estrogens (e.g. liver) should also be considered.

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Section: Discussionmentioning

confidence: 94%

Non-ovarian aromatization is required to activate female sexual motivation in testosterone-treated ovariectomized quail

Bournonville

Balthazart

Ball

et al. 2016

Hormones and Behavior

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“…Numerous animal studies have demonstrated that parietal cells are capable of converting circulating androgens into estrogens, whilst simultaneously expressing CYP19A1 (39–44). Furthermore, the synthesis of E2 through the aromatization of exogenous testosterone has been demonstrated in various GC cell lines (38).…”

Section: Discussionmentioning

confidence: 99%

mRNA expression of steroidogenic enzymes, steroid hormone receptors and their coregulators in gastric cancer

et al. 2017

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Abstract. Epidemiological and experimental findings suggest that the development of gastric cancer (GC) is regulated by steroid hormones. In postmenopausal women and older men, the majority of steroid hormones are produced locally in peripheral tissue through the enzymatic conversion of steroid precursors. Therefore, using reverse transcription-quantitative polymerase chain reaction analysis, the mRNA expression of genes encoding steroidogenic enzymes, including steroid sulfatase (STS), hydroxy-delta-5-steroid dehydrogenase 3 betaand steroid delta-isomerase 1 (HSD3B1), 17β-hydroxysteroid dehydrogenase type 7 and aromatase (CYP19A1), was investigated in primary tumoral and adjacent healthy gastric mucosa from 60 patients with GC. Furthermore, the mRNA levels for estrogen receptor α, estrogen receptor β (ESR2) and androgen receptor (AR), along with their coregulators, including proline, glutamate and leucine rich protein 1, CREB binding protein, nuclear receptor coactivator 1 (NCOA1), nuclear receptor corepressor 1 (NCOR1) and nuclear receptor subfamily 2 group F member 1 (NR2F1), were investigated. Additionally, the association between the mRNA expression of these genes and the clinicopathological features of patients with GC was examined. Significantly decreased levels of STS, HSD3B1, ESR2, AR, NCOA1 and NCOR1 mRNA, in addition to significantly increased levels of CYP19A1 mRNA were demonstrated in tumoral tissue samples compared with adjacent healthy gastric tissue samples. Deregulated expression of these genes in the analyzed tissue samples was associated with certain clinicopathological features of GC, such as age and localization of the tumor. The results of the current study suggest that all of the genes analyzed are expressed in tumoral and adjacent healthy gastric mucosa. In addition, the results indicate that abnormal expression of STS, ESR2, AR, NCOA1 and NCOR1 may serve a role in the development and progression of GC, and may be associated with specific clinicopathological features in patients with GC.

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“…Thus, the consequences of the co-administration of estrogens and SERM at the molecular, cellular and whole body levels are undoubtedly highly complex. Here, our goal was to explore the tissue-specific effects of BZA combined with CE in vivo in mice comparing in two major targets of estrogens, the uterus and the liver (Ahlbory-Dieker et al, 2009, Boverhof et al, 2004, Gao et al, 2008, Gordon et al, 2014, Handgraaf et al, 2013, Kim et al, 2014, Kobayashi et al, 2013, Palierne et al, 2016, Pedram et al, 2013. Our results indicate that the effects of BZA treatment varies according to the duration of treatment (acute versus chronic administration) and the tissue, with the responses observed in the liver being dramatically different from those observed in the uterus.…”

Section: Introductionmentioning

confidence: 95%

The antagonist properties of Bazedoxifene after acute treatment are shifted to stimulatory action after chronic exposure in the liver but not in the uterus

Buscato

Fontaine

Fabre

et al. 2018

Molecular and Cellular Endocrinology

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A promising alternative to conventional hormone therapy for postmenopausal symptoms is treatment combining Bazedoxifene (BZA), a third-generation selective estrogen receptor modulator (SERM), and conjugated equine estrogen (CE). This combination is also known as a tissue-selective estrogen complex (TSEC). Understanding the tissue-specific actions of SERMs and the TSEC remains a major challenge to try to predict their clinical effects. The aim of this study was to compare acute versus chronic treatment with BZA, CE or CE + BZA in two major targets of estrogens, the uterus and the liver. In these two tissues, acute treatment with CE, but not with BZA, induced similar gene expression change than the most important endogenous estrogen, 17-β estradiol (E2). Acute induction of gene expression by E2 or by CE was antagonized by the addition of BZA. Concomitantly, BZA alone or in combination with E2 or CE induced a partial degradation of ERα protein after acute exposure. In uterus, chronic treatment of BZA alone had no impact on tissue weight gain or on epithelial cell proliferation, and also antagonized CE-effect in uterus, thereby mimicking the acute effect. By contrast, in the liver, chronic BZA and CE + BZA elicited agonistic transcriptional effects similar to those of CE alone. In addition, at variance to BZA acute effect, no change in ERα protein abundance was observed after chronic treatment in this tissue. These experimental in vivo data highlight a new aspect of the time-dependent tissue-specific action of BZA or TSEC, i.e. they can act acutely as antagonists but become agonists after chronic treatment. This shift was observed in liver tissue, but not in proliferative sex target such as the uterus.

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Gastric estradiol-17β (E2) and liver ERα correlate with serum E2 in the cholestatic male rat

Cited by 19 publications

References 34 publications

Non-ovarian aromatization is required to activate female sexual motivation in testosterone-treated ovariectomized quail

Non-ovarian aromatization is required to activate female sexual motivation in testosterone-treated ovariectomized quail

mRNA expression of steroidogenic enzymes, steroid hormone receptors and their coregulators in gastric cancer

The antagonist properties of Bazedoxifene after acute treatment are shifted to stimulatory action after chronic exposure in the liver but not in the uterus

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