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Choline Modulates Soluble‐Endoglin (sEng) and Vascular Endothelial Growth Factor (VEGF) in Cultured Human Placental Trophoblasts
Author(s) -
Andrew Benjamin Yates,
Jiang Xinyin,
Jones Sara,
Caudill Marie A,
Bran Patsy M
Publication year - 2013
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.27.1_supplement.1077.7
Subject(s) - choline , endocrinology , medicine , vascular endothelial growth factor , preeclampsia , chemistry , placental growth factor , vegf receptors , andrology , biology , pregnancy , genetics
Altering the balance between the anti‐angiogenic factors, soluble fms‐related tyrosine kinase‐1 (sFLT1) and sEng, and the angiogenic factors, VEGF and transforming growth factor beta (TGF‐β), contributes to preeclampsia (PE) and persistence of hypoxia (Hx). Increasing sFLT1 and sEng may sequester VEGF and TGF‐β. Recently we showed that supplemental choline reduced placental sFLT1 mRNA and maternal plasma sFLT1 in pregnant women and cultured trophoblasts (HTR‐8/SVneo). To determine if choline regulates sEng production and VEGF gene expression independently or interactively with Hx, HTR‐8/SVneo cells were cultured in a 2×4 factorial design in either normoxia (20% O 2 , Nx) or Hx (1% O 2 ) and 13 μM, 18 μM, 28 μM (control) or 48 μM for 96 hours. Results were analyzed by 2‐way ANOVA (SigmaPlot). Low choline (13 μM) under Nx, but not Hx, increased media sEng (14%, p=0.036) and mRNA levels of VEGF (160.9%, p<0.001), HIF‐1α (36.2%, p<0.001) and HIF‐2α (63.3%, p<0.001) compared to control. Hx also increased media sEng (9.25%, p<0.001) and VEGF mRNA levels (114.18%, p<0.001) across all choline levels. Thus, low choline modulates, under Nx but not Hx, the anti‐angiogenic sEng as well as the angiogenic VEGF, thereby mimicking the effects of Hx. Low choline under Nx, therefore, may alter the resulting balance of antiangiogenic and angiogenic factors contributing to PE. Funded by USDA NIFA AFRI003397