Expression and activity of vitamin D receptor in the human placenta and in choriocarcinoma BeWo and JEG-3 cell lines

Pospěchová, Kateřina; Rozehnal, Veronika; Stejskalová, Lucie; Vrzal, Radim; Pospisilova, Nada; Jamborova, Gabriela; May, Karen; Siegmund, Werner; Dvořák, Zdeněk; Nachtigal, Petr; Semecký, Vladimír; Pávek, Petr

doi:10.1016/j.mce.2008.12.003

Cited by 72 publications

(58 citation statements)

References 44 publications

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“…Similar epigenetic suppression of VDR mRNA expression has been demonstrated in placental and choriocarcinoma cell lines, which also showed VDR mRNA re-expression after AZA treatment. 18 Our initial proliferation assays confirmed the relative Calcitriol insensitivity in breast cancer cells (see Fig. 2A), and an additive antiproliferative response to combined Calcitriol and AZA treatment.…”

Section: Discussionsupporting

confidence: 66%

DNA methylation-related vitamin D receptor insensitivity in breast cancer

Marik

Fackler

Gabrielson

et al. 2010

Cancer Biology & Therapy

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Section: Discussionsupporting

confidence: 66%

DNA methylation-related vitamin D receptor insensitivity in breast cancer

Marik

Fackler

Gabrielson

et al. 2010

Cancer Biology & Therapy

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“…Expression of hCG is elevated by cAMP in trophoblast cells, and this was associated with decreased expression of CYP27B1, with VDR expression being unaffected (Avila et al 2007), suggesting that presence of the vitamin D metabolic and signaling pathways in the placenta is differentiation sensitive. The JEG-3 trophoblast cell line has also been reported to express CYP27B1, but synthesis of 1,25(OH) 2 D by these cells appears to be significantly less than that observed with primary trophoblast cells and unaffected by cAMP (Pospechova et al 2009). In addition to cAMP, inflammatory cytokines (Noyola-Martinez et al 2014) and insulin-like growth factor I (Halhali et al 1999) also stimulate trophoblast expression of CYP27B1 and synthesis of 1,25(OH) 2 D.…”

Section: Vitamin D Metabolism and Function In Trophoblast Cellsmentioning

confidence: 97%

“…Primary cultures of human syncytiotrophoblast express CYP27B1 and are able to synthesize 1,25(OH) 2 D (Diaz et al 2000) and also express VDR (Pospechova et al 2009 this may be due to epigenetic suppression of VDR in these cells (Pospechova et al 2009). Further studies to assess the impact of differentiation of cultured trophoblast cells have been carried out using cyclic AMP (cAMP) to mimic the process of syncytialization (Keryer et al 1998).…”

Section: Vitamin D Metabolism and Function In Trophoblast Cellsmentioning

confidence: 99%

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

Ganguly

Tamblyn

Finn-Sell

et al. 2018

Journal of Endocrinology

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Pregnancy is associated with significant changes in vitamin D metabolism, notably increased maternal serum levels of active vitamin D, 1,25-dihydroxyvitamin (1,25(OH) 2 D). This appears to be due primarily to increased renal activity of the enzyme 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) that catalyzes synthesis of 1,25(OH) 2 D, but CYP27B1 expression is also prominent in both the maternal decidua and fetal trophoblast components of the placenta. The precise function of placental synthesis of 1,25(OH) 2 D remains unclear, but is likely to involve localized tissue-specific responses with both decidua and trophoblast also expressing the vitamin D receptor (VDR) for 1,25(OH) 2 D. We have previously described immunomodulatory responses to 1,25(OH) 2 D by diverse populations of VDR-expressing cells within the decidua. The aim of the current review is to detail the role of vitamin D in pregnancy from a trophoblast perspective, with particular emphasis on the potential role of 1,25(OH) 2 D as a regulator of trophoblast invasion in early pregnancy. Vitamin D deficiency is common in pregnant women, and a wide range of studies have linked low vitamin D status to adverse events in pregnancy. To date, most of these studies have focused on adverse events later in pregnancy, but the current review will explore the potential impact of vitamin D on early pregnancy, and how this may influence implantation and miscarriage.

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“…Human placenta and decidua are capable of producing and secreting 1,25(OH) 2 D 3 (38). The existence of gene transcript of 1␣-hydroxylase and the finding of VDR expression in placental trophoblasts suggest a possible autocrine loop of vitamin D signaling within trophoblasts (12,27). A study by Zehnder et al (41) also found that mRNA expression of 1␣-hydroxylase was higher in the first-and secondtrimester than in the third-trimester placentas, whereas mRNA expressions for VDR across gestation were less pronounced compared with 1␣-hydroxylase.…”

mentioning

confidence: 99%

Expressions of vitamin D metabolic components VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR in placentas from normal and preeclamptic pregnancies

Zhao

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

135

108

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Vitamin D insufficiency/deficiency during pregnancy has been linked to increased risk of preeclampsia. Placenta dysfunction plays an important role in the pathogenesis of this pregnancy disorder. In this study, we tested the hypothesis that disturbed vitamin D metabolism takes place in preeclamptic placentas. Protein expressions of vitamin D binding protein (VDBP), 25-hydroxylase (CYP2R1), 1␣-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), and vitamin D receptor (VDR) were examined in placentas from normotensive and preeclamptic pregnancies. By immunostaining we found that in normal placenta VDBP, CYP24A1, and VDR expressions are localized mainly in trophoblasts, whereas CYP2R1 and CYP27B1 expressions are localized mainly in villous core fetal vessel endothelium. Protein expressions of CYP2R1 and VDR are reduced, but CYP27B1 and CYP24A1 expressions are elevated, in preeclamptic compared with normotensive placentas. Because increased oxidative stress is an underlying pathophysiology in placental trophoblasts in preeclampsia, we further determined whether oxidative stress contributes to altered vitamin D metabolic system in placental trophoblasts. Trophoblasts isolated from normal-term placentas were treated with hypoxic-inducing agent CoCl 2, and protein expressions of VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR were determined. We found that hypoxia-induced downregulation of VDBP, CYP2R1, and VDR and upregulation of CYP27B1 and CYP24A1 expressions were consistent with that seen in preeclamptic placentas. CuZnSOD expression was also downregulated in trophoblasts treated with CoCl 2. These results provide direct evidence of disrupted vitamin D metabolic homeostasis in the preeclamptic placenta and suggest that increased oxidative stress could be a causative factor of altered vitamin D metabolism in preeclamptic placentas. Vitamin D status during pregnancy has been drawing great attention (19,22,32,39). Studies have shown that sufficient vitamin D intake during pregnancy reduces the risk of complications, including gestational diabetes, preterm birth, and infection (8, 36). Conversely, vitamin D deficiency during pregnancy has been linked to several adverse pregnancy outcomes (19,22,32,39), including those associated with placental insufficiency such as preeclampsia and low birth weight (8,36). Maternal 25(OH)D 3 levels are lower in women with preeclampsia than in normotensive pregnant women (1, 7). Moreover, a nested case control study revealed that maternal vitamin D deficiency at less than 22 wk of gestation is a strong, independent risk factor for preeclampsia (7). The finding of the association of maternal vitamin D deficiency and increased risk of preeclampsia (3,7,28,29) further emphasizes the importance of adequate vitamin D levels and proper vitamin D metabolism during pregnancy.Normal placental development and function ensure a healthy pregnancy outcome. It is believed that during pregnancy, 1,25(OH) 2 D 3 may be produced not only by kidneys but also by placenta trophoblasts. Human placenta and decidua are c...

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Expression and activity of vitamin D receptor in the human placenta and in choriocarcinoma BeWo and JEG-3 cell lines

Cited by 72 publications

References 44 publications

DNA methylation-related vitamin D receptor insensitivity in breast cancer

DNA methylation-related vitamin D receptor insensitivity in breast cancer

Vitamin D, the placenta and early pregnancy: effects on trophoblast function

Expressions of vitamin D metabolic components VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR in placentas from normal and preeclamptic pregnancies

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