Progesterone receptor expression in the human placenta

Shanker, Y. Gopi; Rao, A Jagannadha

doi:10.1093/molehr/5.5.481

Cited by 29 publications

(14 citation statements)

References 27 publications

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“…6A), which is consistent with the human data of a previous study in which PR expression (both protein and mRNA) was shown to be much higher in first-trimester human placenta than in term placenta (31). The mechanisms by which the expression of nuclear receptors is regulated by pregnancy are not known but may be related to pregnancyspecific hormones, since some of these nuclear receptors such as AhR and HIF1␣ have already been shown to be regulated by pregnancy-specific hormones such as progesterone and 17␤-estradiol (4,10,31). When compared with Bcrp1 expression, we found significant correlations of Bcrp1 mRNA with HIF1␣, AhR, and ER␤ mRNA in placenta, with HIF1␣ mRNA in kidney, and with AhR and ER␣ mRNA in liver (Table 1 and Fig.…”

Section: Discussionsupporting

confidence: 92%

Expression of the breast cancer resistance protein (Bcrp1/Abcg2) in tissues from pregnant mice: effects of pregnancy and correlations with nuclear receptors

Wang

Hudkins

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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The breastcancer resistance protein (BCRP) plays an important role in drug disposition, including limiting drug penetration across the placental barrier. Our goal was to investigate the effects of pregnancy on Bcrp1 expression in pregnant mice. We examined Bcrp1 expression in placenta, kidney, liver, and small intestine at various gestational ages. Bcrp1 protein levels peaked at gestation day ( gd) 15 in placenta, at gd 10 and 15 in kidney, and at gd 15 in liver; however, Bcrp1 protein levels in small intestine did not change significantly with gestational ages. Immunohistochemistry analysis revealed that the cellular localization of Bcrp1 in placenta, kidney, liver, and small intestine was not influenced by pregnancy. Bcrp1 mRNA levels were analyzed by quantitative real-time RT-PCR. In general, the effects of pregnancy on Bcrp1 protein somewhat lagged behind the effects on Bcrp1 mRNA. To further investigate the possible roles of nuclear receptors in the regulation of the Bcrp1 gene during pregnancy, we examined mRNA levels of aryl hydrocarbon receptor (AhR), hypoxia-inducible factor 1α (HIF1α), estrogen receptor α (ERα), estrogen receptor β (ERβ), or progesterone receptor and compared them with those of Bcrp1. Bcrp1 mRNA was significantly correlated with mRNA of AhR, HIF1α, and ERβ in placenta, with mRNA of HIF1α in kidney, and with mRNA of AhR and ERα in liver. These data suggest that Bcrp1 expression in mouse tissues can be altered by pregnancy in a gestational age-dependent manner. Such effects are likely mediated by certain nuclear receptors through a transcriptional mechanism.

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Section: Discussionsupporting

confidence: 92%

Expression of the breast cancer resistance protein (Bcrp1/Abcg2) in tissues from pregnant mice: effects of pregnancy and correlations with nuclear receptors

Wang

Hudkins

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…However, there is some controversy as to whether the PR is expressed in placental trophoblasts. Several studies have not been able to detect PR in the placenta [18,27,28], whereas a number of other studies have [19,20]. PR exists in human as two proteins, PR-A and PR-B, encoded by a single gene.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Karalis et al [18] concluded that P4 downregulation of CRH gene expression in placenta occurred through the glucocorticoid receptor (GR) because they did not detect P4 receptor (PR) expression in placental cells. However, several studies have shown that the PR is expressed by placental cells [19,20]. Thus the mechanisms by which P4 could inhibit placental CRH production are unclear.…”

mentioning

confidence: 99%

Progesterone receptors A and B differentially modulate corticotropin-releasing hormone gene expression through a cAMP regulatory element

Hou

Yang

et al. 2004

Cellular and Molecular Life Sciences (CMLS)

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Corticotrophin-releasing hormone (CRH) plays a major role in mechanisms controlling human pregnancy and parturition. Gene regulation by progesterone may be a key point in the control of placental CRH production. Studies in primary placental cells show that antagonism of progesterone activity or production by RU486 or trilostane leads to an increase in CRH promoter activity. This effect can be reversed by the addition of progesterone. Overexpression of progesterone receptor A (PR-A) or glucocorticoid receptor resulted in a decrease in CRH promoter activity following progesterone treatment, whereas an increase in promoter activity was observed with overexpressed PR-B. Studies including mutation of the cAMP regulatory element (CRE) confirm this site to be essential for the progesterone-mediated effects. In summary, our results demonstrate that progesterone regulates CRH gene transcription via a CRE in the CRH promoter and that PR-A and PR-B exhibit different actions in the regulation of CRH gene expression.

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“…They also show that these increases in uptake can be attributed to increased NIS expression in the placental cultures upregulated in response to incubation with those hormones. The ability of pregnancy-related hormones to influence 125 I uptake and NIS expression is obviously dependent on the presence and abundance of individual hormone receptors in late pregnancy placentas [31,32,33,34]. …”

Section: Discussionmentioning

confidence: 99%

Regulation of Iodide Uptake in Placental Primary Cultures

2013

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Background: Maintenance of adequate iodide supply to the developing fetus is dependent not only on maternal dietary iodine intake but also on placental iodide transport. The objective of this study was to examine the effects of different pregnancy-associated hormones on the uptake of radioiodide by the placenta and to determine if iodide transporter expression is affected by hormone incubation. Methods: Primary cultures of placental trophoblast cells were established from placentas obtained at term from pre-labor caesarean sections. They were pre-incubated with 17β-estradiol, prolactin, oxytocin, human chorionic gonadotropin (hCG) and progesterone either singly or in combination over 12 h with ¹²⁵I uptake being measured after 6 h. RNA was isolated from placental trophoblasts and real-time RT-PCR performed using sodium iodide symporter (NIS) and pendrin (PDS) probes. Results: Significant dose response increments in ¹²⁵I uptake by trophoblast cells (p < 0.01) were observed following incubation with hCG (60% increase), oxytocin (45% increase) and prolactin (32% increase). Although progesterone (50-200 ng/ml) and 17β-estradiol (1,000-15,000 pg/ml) alone produced no significant differences in uptake, they facilitated increased uptake when combined with prolactin or oxytocin, with a combination of all four hormones producing the greatest increase (82%). Increased ¹²⁵I uptake was accompanied by corresponding increments in NIS mRNA (ratio 1.52) compared to untreated control cells. No significantly increased expression levels of PDS were observed. Conclusions: Pregnancy-associated hormones, particularly oxytocin and hCG, have a role in promoting placental iodide uptake which may protect the fetus against iodine deficiency.

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Progesterone receptor expression in the human placenta

Cited by 29 publications

References 27 publications

Expression of the breast cancer resistance protein (Bcrp1/Abcg2) in tissues from pregnant mice: effects of pregnancy and correlations with nuclear receptors

Expression of the breast cancer resistance protein (Bcrp1/Abcg2) in tissues from pregnant mice: effects of pregnancy and correlations with nuclear receptors

Progesterone receptors A and B differentially modulate corticotropin-releasing hormone gene expression through a cAMP regulatory element

Regulation of Iodide Uptake in Placental Primary Cultures

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