Expression profiling of vitamin D receptor in placenta, decidua and ovary of pregnant mice

Shahbazi, Mehdi; Jeddi-Tehrani, Mahmood; Zareie, Mehri; Salek-Moghaddam, Alireza; Akhondi, Mohammad Mehdi; Bahmanpoor, M.; Sadeghi, Mohammad Reza; Zarnani, Amir‐Hassan

doi:10.1016/j.placenta.2011.06.013

Cited by 76 publications

(54 citation statements)

References 39 publications

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“…12 Animal models have shown that vitamin D induces ovarian steroidogenesis. Vitamin D increased dehydroepiandrosterone sulfotranserase (SULT2A1) transcription, an enzyme that mediates sulfo-conjugation of endogenous hydroxysteroids.…”

Section: In Animal Cellsmentioning

confidence: 99%

Vitamin D and aspects of female fertility

Voulgaris

Papanastasiou

Piaditis

et al. 2017

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The role of vitamin D in female reproduction has been intensively examined over the last few decades. A large body of evidence suggests that vitamin D might have beneficial effects on metabolic/hormonal parameters of PCOS and endometriosis, while it appears to be associated with IVF outcomes. However, due to the heterogeneity among observational and interventional studies, no cause-effect relationship has yet been established. The aim of this review is to analyze recent in vitro animal and human studies which examined the association of vitamin D with disease entities affecting female fertility potential. Recent research data strongly imply that vitamin D is implicated in female reproduction and might represent a beneficial and inexpensive therapeutic approach, in combination with first-line medical treatments, to female infertility.

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Section: In Animal Cellsmentioning

confidence: 99%

Vitamin D and aspects of female fertility

Voulgaris

Papanastasiou

Piaditis

et al. 2017

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“…However, as with many steroid hormones, vitamin D can also exert rapid non-genomic effects, likely via VDR located within the plasma membrane (Norman et al 2002, Menegaz et al 2011. VDR is also abundantly expressed in placental tissue, thus allowing for localized placental 1,25(OH) 2 D binding and subsequent gene transcription (Shahbazi et al 2011). Interestingly, the precursor 25-(OH)D readily crosses the placenta; however, 1,25(OH) 2 D is unable to be transported across the placenta, and thus is found in relatively low levels in fetal circulation (Kovacs 2008).…”

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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“…14 Furthermore, Shahbazi study mention that the rationale behind placental VDR expression was unclear, but it had a role in the physiological processes such as absorption of calcium and its transition to the developing fetus before delivery. 15 Newborn size had important implications for mortality, morbidity, subsequent growth and development. There were overwhelmingly more cases of LBW in developing countries than in developed countries.…”

Section: Discussionmentioning

confidence: 99%