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Placenta Vitamin D Signaling in Preeclampsia
Author(s) -
Wheeler Carol,
Benoit Joseph N,
Anderson Cindy M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.629.3
Subject(s) - calcitriol receptor , placenta , vitamin d and neurology , preeclampsia , western blot , fetus , vitamin d deficiency , pregnancy , medicine , vitamin , endocrinology , paracrine signalling , retinoid x receptor , andrology , biology , receptor , biochemistry , genetics , nuclear receptor , gene , transcription factor
National trends demonstrate that an overall increase in the prevalence of vitamin D insufficiency is associated with risk for preeclampsia (PE), particularly among those with reduced sun exposure. Previous studies in our lab demonstrated that 70% of women pregnant with their first baby living in the northern plains had pregnancies complicated by hypovitaminosis D and that 24% of the study participants experienced PE. As the placenta produces and utilizes vitamin D in a paracrine fashion, we investigated the differences in expression of key proteins involved in vitamin D signaling in placentas from women with normotensive pregnancy (NP) and in PE. Placenta samples were collected after delivery and frozen for analysis of protein expression by Western blot analysis. Lysates from placental homogenates were subjected to electrophoresis, transferred to a PVDF membrane and incubated with antibodies against 1á‐hydroxyase (CYP27B1), vitamin D (VDR) and retinoid X (RXR) receptors. There were no significant differences in expression of VDR or RXR between groups. Expression of CYP27B1 was significantly increased in PE compared to NP (p<0.05). Our findings indicate that placental conversion of the circulating form of vitamin D to the active form is increased in preeclampsia, increasing availability of vitamin D for utilization by the placental‐fetal unit. Supported by Robert Wood Johnson Foundation, APS.