Mechanisms of homocysteine transport by human placenta:Relationship to placental vascular distensibility and birthweight

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Low birthweight (LBW) infants are at greater risk of developmental delay and cerebral palsy in later childhood than those of normal birthweight. In adult life, LBW may predispose to cardiovascular disease. This may be linked to a higher concentration of an amino acid called homocysteine which damages blood vessel walls. In pregnancy, sub-optimal folate or vitamin B12 status may contribute to raised homocysteine concentrations in maternal plasma and reduced fetal growth. How homocysteine is transported by the placenta is unknown. It is possible that homocysteine-induced damage to placental blood vessels provides a causative link between impaired placental function and LBW. Our project will identify transport systems that carry homocysteine across the placenta in normal pregnancies and investigate whether these transporters are modulated by the vitamins folate and B12, micronutrients important in the metabolic conversion of homocysteine. We plan to explore relationships between homocysteine concentrations in cord blood, normal variations in infant size at birth, and the distensible properties of placental arterial vessels as a model of fetal vessels in which vascular function can be examined. We hope that our work will lead to new initiatives together with a continuum of care to improve fetal growth and health of newborn infants.