Decreased placental vitamin D receptor contributes to aberrant cell-cycle gene regulation in human idiopathic fetal growth restriction

Nguyen, Tony; Yong, Hannah; Borg, Anthony J.; Brennecke, Shaun; Murthi, Padma

doi:10.1016/j.placenta.2015.07.318

Cited by 2 publications

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“…Proliferation or cell division goes through cell growth and DNA synthesis phases, which are mediated by checkpoints to ensure the cell's fidelity. In our most recent study, (Nguyen et al, 2015b ), we identified TGFβ-3, a known inhibitor of cell cycle progression through G1 phase (Caniggia et al, 1999 ), as a candidate downstream target gene of VDR. Indeed, TGFβ-3 mRNA and protein expression were significantly decreased in placentae from idiopathic FGR-affected pregnancies compared to control placentae.…”

Section: Downstream Targets Of Vdr In the Placentamentioning

confidence: 99%

Role of the Placental Vitamin D Receptor in Modulating Feto-Placental Growth in Fetal Growth Restriction and Preeclampsia-Affected Pregnancies

et al. 2016

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Fetal growth restriction (FGR) is a common pregnancy complication that affects up to 5% of pregnancies worldwide. Recent studies demonstrate that Vitamin D deficiency is implicated in reduced fetal growth, which may be rescued by supplementation of Vitamin D. Despite this, the pathway(s) by which Vitamin D modulate fetal growth remains to be investigated. Our own studies demonstrate that the Vitamin D receptor (VDR) is significantly decreased in placentae from human pregnancies complicated by FGR and contributes to abnormal placental trophoblast apoptosis and differentiation and regulation of cell-cycle genes in vitro. Thus, Vitamin D signaling is important for normal placental function and fetal growth. This review discusses the association of Vitamin D with fetal growth, the function of Vitamin D and its receptor in pregnancy, as well as the functional significance of a placental source of Vitamin D in FGR. Additionally, we propose that for Vitamin D to be clinically effective to prevent and manage FGR, the molecular mechanisms of Vitamin D and its receptor in modulating fetal growth requires further investigation.

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Section: Downstream Targets Of Vdr In the Placentamentioning

confidence: 99%

Role of the Placental Vitamin D Receptor in Modulating Feto-Placental Growth in Fetal Growth Restriction and Preeclampsia-Affected Pregnancies

et al. 2016

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“…A recent study shows that placental VDR expression is downregulated in pregnancies complicated by fetal growth restriction (Nguyen et al 2015b) and is associated with abnormal trophoblast expression of cell-cycle regulatory genes in vitro (Nguyen et al 2015a). This indicates that placental vitamin D metabolism regulates fetal growth and development; however, relatively little is known of the mechanisms behind such regulatory processes, and whether they may be compromised during vitamin D-deficient pregnancies.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency and impaired placental function: potential regulation by glucocorticoids?

Yates¹,

Crew²,

Wyrwoll³

2017

Reproduction

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Maternal vitamin D deficiency has been implicated in a range of pregnancy complications including preeclampsia, preterm birth and intrauterine growth restriction. Some of these adverse outcomes arise from alterations in placental function. Indeed, vitamin D appears critical for implantation, inflammation, immune function and angiogenesis in the placenta. Despite these associations, absence of the placental vitamin D receptor in mice provokes little effect. Thus, interactions between maternal and fetal compartments are likely crucial for instigating adverse placental changes. Indeed, maternal vitamin D deficiency elicits changes in glucocorticoid-related parameters in pregnancy, which increase placental and fetal glucocorticoid exposure. As in utero glucocorticoid excess has a well-established role in eliciting placental dysfunction and fetal growth restriction, this review proposes that glucocorticoids are an important consideration when understanding the impact of vitamin D deficiency on placental function and fetal development.Reproduction (2017) 153 R163-R171

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Decreased placental vitamin D receptor contributes to aberrant cell-cycle gene regulation in human idiopathic fetal growth restriction

Cited by 2 publications

References 0 publications

Role of the Placental Vitamin D Receptor in Modulating Feto-Placental Growth in Fetal Growth Restriction and Preeclampsia-Affected Pregnancies

Role of the Placental Vitamin D Receptor in Modulating Feto-Placental Growth in Fetal Growth Restriction and Preeclampsia-Affected Pregnancies

Vitamin D deficiency and impaired placental function: potential regulation by glucocorticoids?

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