Abstract
This study explored the role of choline in placental vascular function. In a 12‐week controlled feeding study among third trimester pregnant women, the higher choline intake group (930 vs. 480 mg/d) had lower (P=0.05) placental and circulating levels of soluble fms‐like tyrosine kinase‐1 (sFLT1), an anti‐angiogenic factor that predicts preeclampsia risk. The effect of choline on placental cell function was further investigated using immortalized HTR‐8/SVneo trophoblasts cultured in different choline concentrations (28, 13 and 8 μM) for 96 hours. The decrease in choline concentrations led to a graded increase (P<0.01) in the gene expression and secretion of sFLT1, expression of the proinflammatory markers [e.g. interleukin 1 beta (IL1B)], apoptosis and oxidative stress. Cellular phosphatidylcholine dramatically decreased (50%, P<0.01) in the lower choline group, whereas the protein kinase C (PKC) isoforms δ and ε, activated by breakdown products of phosphatidylcholine, increased (P<0.01). The addition of a PKC inhibitor partially rescued the increased expression of sFLT1 and apoptosis. In conclusion, choline influences placental vascular function partially via PKC.Grant Funding Source: USDA NIFA AFRI003397
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