Placental Vitamin D-Binding Protein Expression in Human Idiopathic Fetal Growth Restriction.

Alice F Wookey,Harry M Georgiou,Shaun P Brennecke,Bill Kalionis,Hannah E J Yong,Padma Murthi,Tejasvy Chollangi

doi:10.1155/2017/5120267

Alice F Wookey, Harry M Georgiou + Show 5 more

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https://doi.org/10.1155/2017/5120267

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Abstract

Vitamin D-binding protein is a multifunctional serum protein with multiple actions related to normal health. Vitamin D-binding protein transports vitamin D and influences the metabolism of this key hormone but it also has additional immunomodulatory and actin-clearing properties. We investigated whether vitamin D-binding protein expression is altered in fetal growth restriction-associated placental dysfunction. Protein was extracted from 35 placentae derived from 17 healthy control subjects and 18 gestation-matched subjects with fetal growth restriction (FGR). FGR subjects were further subdivided as idiopathic (n = 9) and nonidiopathic (n = 9). Vitamin D-binding protein and 25(OH) vitamin D were measured by ELISA and normalized to protein concentration. The results showed significantly reduced levels of placental vitamin D-binding protein (control versus FGR, p < 0.05, Student's t-test) that were strongly associated with idiopathic fetal growth restriction (p < 0.01, Kruskal-Wallis), whereas levels of vitamin D-binding protein were not associated with placental 25(OH) vitamin D stores (p = 0.295, Pearson's correlation). As such, vitamin D-binding protein may be a factor in unexplained placental dysfunction associated with idiopathic fetal growth restriction and may potentially serve as a biomarker of this disease.

Highlights

Fetal growth restriction (FGR) is a significant public health problem, because of its association with perinatal mortality and long-term metabolic disease
This study is the first to demonstrate significantly reduced placental vitamin D-binding protein (VDBP) concentration in pregnancies complicated by fetal growth restriction (FGR) compared to uncomplicated pregnancies (p < 0.05; Figure 1(a))
These data suggest that reduced VDBP is most pronounced in the idiopathic FGR subgroup (p < 0.01; Figure 1(b))

Summary

Introduction

Fetal growth restriction (FGR) is a significant public health problem, because of its association with perinatal mortality and long-term metabolic disease. Whilst well established risk factors (e.g., maternal hypertension, toxin exposure, and fetal genetic abnormalities) are identifiable in some cases of FGR, most arise from unexplained placental dysfunction caused by unknown insults during placental development and are categorized as “idiopathic” [1]. Many observational studies link FGR with low levels of vitamin D [2], which is a critical hormone in placental development and function. Vitamin D acts as a key regulator of implantation, inflammation, and production of important pregnancy hormones [3]. VDBP regulates global placental function and acts as a determinant of fetal nutrient delivery and long-term metabolic programming [6]

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