Human 17 -Hydroxysteroid Dehydrogenase Type 2 Messenger Ribonucleic Acid Expression and Localization in Term Placenta and in Endometrium during the Menstrual Cycle

Mustonen, Mika

doi:10.1210/jc.83.4.1319

Cited by 48 publications

(33 citation statements)

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“…Similar findings have been reported by several other investigators (11)(12)(13). 17␤HSD2 is localized exclusively in the glandular epithelial cells as demonstrated by immunohistochemistry (14) and in situ hybridization (15).…”

supporting

confidence: 92%

Progesterone Induction of 17β-Hydroxysteroid Dehydrogenase Type 2 during the Secretory Phase Occurs in the Endometrium of Estrogen-Dependent Benign Diseases But Not in Normal Endometrium

Kitawaki¹,

Koshiba²,

Ishiga³

et al. 2000

The Journal of Clinical Endocrinology & Metabolism

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In the human endometrium, inactivation of 17␤-estradiol to estrone is catalyzed by 17␤-hydroxysteroid dehydrogenase type 2 (17␤HSD2). Previous studies have shown that the 17␤HSD2 activity in the endometrium is elevated during the secretory phase, as compared with the level during the proliferative phase, and that the elevation is in response to progesterone via the progesterone receptors. Recently, it has been demonstrated that aromatase cytochrome P450, the enzyme responsible for estrogen biosynthesis, is not present in the endometrium obtained from normal menstruating women with cervical cancer in situ showing no other gynecological disease (defined as "disease free"), but present in the endometrium obtained from patients with endometriosis, adenomyosis, and/or leiomyomas (defined as "diseased"). However, the previous 17␤HSD studies have been performed without distinguishing between disease-free and diseased endometria. We, therefore, analyzed 17␤HSD2 distinguishing between disease-free and diseased endometria. During the proliferative phase, the abundance of messenger RNA (mRNA) and activity of 17␤HSD2 were comparable in both disease-free and diseased endometrium. However, during the secretory phase, while the abundance of mRNA and activity of 17␤HSD2 increased 4-to 6-fold in diseased endometrium, the 17␤HSD2 remained unchanged in the disease-free endometrium. Kinetic studies showed that the K m was identical among the four groups of endometria, suggesting that the elevation of 17␤HSD2 simply resulted from increased mRNA transcription. Organ culture of proliferative endometria in the presence of progestins resulted in the stimulation of 17␤HSD2 in diseased endometria via the progesterone receptors, whereas disease-free endometrium was not stimulated by progestins. These results suggest that the previous paradigm that 17␤HSD2 activity in the endometrium is elevated during the secretory phase is confined to diseased endometrium but not to disease-free endometrium and that the estrogen metabolism is altered in the endometria of the patients with estrogen-dependent benign diseases. (J Clin Endocrinol Metab 85: 3292-3296, 2000)

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supporting

confidence: 92%

Progesterone Induction of 17β-Hydroxysteroid Dehydrogenase Type 2 during the Secretory Phase Occurs in the Endometrium of Estrogen-Dependent Benign Diseases But Not in Normal Endometrium

Kitawaki¹,

Koshiba²,

Ishiga³

et al. 2000

The Journal of Clinical Endocrinology & Metabolism

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“…In fact, interconversion activity has been reported in endometrial tissue (21). Expression of type 2 17h-hydroxysteroid dehydrogenases has been reported in glandular epithelial cells of cancer-free and malignant endometrium, whereas expression of type 1 17h-hydroxysteroid dehydrogenases has not been detected (22,23). The expression of other types of 17h-hydroxysteroid dehydrogenases has not h-hydroxysteroid dehydrogenases function in normal and cancer tissues of the endometrium remain to be determined.…”

Section: Discussionmentioning

confidence: 99%

Aromatase Expression in Stromal Cells of Endometrioid Endometrial Cancer Correlates with Poor Survival

Segawa

Shozu

Murakami

et al. 2005

Clinical Cancer Research

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“…Indeed, we previously showed that 17bHSD2 mRNA level is higher in total villi samples from term placentas than from mid-gestation placentas, and that 17bHSD2 in endothelial cells of the villi might control the amount of active and inactive estrogens in the fetal circulation [10]. In addition, a higher abundance of 17bHSD2 in the endothelium of umbilical arteries at term also suggests that this enzyme could minimize the fetal contribution to the maternal rise in E 2 levels and also control the transfer of fetal androgens into the maternal circulation therefore, contributing to protect the maternal system against inappropriate androgenic effects [41,42].…”

Section: Discussionmentioning

confidence: 99%

Human type 2 17beta-hydroxysteroid dehydrogenase in umbilical vein and artery endothelial cells: differential inactivation of sex steroids according to the vessel type

et al. 2011

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The human placenta produces high amounts of estradiol. 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) is expressed by placental endothelial cells and was proposed to regulate sex hormone levels. Previous results obtained in term placenta suggested that 17βHSD2 expression and activity differ among umbilical cord vessels. In this study, 17βHSD2 expression level and enzymatic activity, and estrogen receptor α and β expression levels, were measured in endothelial cell cultures from umbilical arteries (HUAEC) and vein (HUVEC) using real-time quantitative PCR, western blot, and radiolabeled steroids. 17βHSD2-specific activities were also measured in proximal and distal segments of freshly isolated umbilical cord arteries and vein. 17βHSD2 mRNA level and activity were higher in HUAEC than in HUVEC. Activity was higher in umbilical arteries than in the umbilical vein. In arteries, enzymatic activity was higher near the placenta, suggesting a gradient of expression. No difference was found in ERα expression, whereas ERβ was expressed at a higher level in HUAEC than in HUVEC. Expression profiles of estrogen receptors and 17βHSD2 suggest a vessel type-specific response to estrogens. Our data support a differential modulation of biologically active sex steroid levels according to the vessel type in the foeto-placental unit, with apparent higher inactivation in the arterial system.

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Human 17 -Hydroxysteroid Dehydrogenase Type 2 Messenger Ribonucleic Acid Expression and Localization in Term Placenta and in Endometrium during the Menstrual Cycle

Cited by 48 publications

References 0 publications

Progesterone Induction of 17β-Hydroxysteroid Dehydrogenase Type 2 during the Secretory Phase Occurs in the Endometrium of Estrogen-Dependent Benign Diseases But Not in Normal Endometrium

Progesterone Induction of 17β-Hydroxysteroid Dehydrogenase Type 2 during the Secretory Phase Occurs in the Endometrium of Estrogen-Dependent Benign Diseases But Not in Normal Endometrium

Aromatase Expression in Stromal Cells of Endometrioid Endometrial Cancer Correlates with Poor Survival

Human type 2 17beta-hydroxysteroid dehydrogenase in umbilical vein and artery endothelial cells: differential inactivation of sex steroids according to the vessel type

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