Research Line

Gestational diabetes are characterized by abnormal D-glucose metabolism and hyperglycaemia, and induce foetal endothelial dysfunction with implications in adult life increasing the risk of vascular diseases. Uptake of adenosine (a vasoactive endogenous nucleoside) by the umbilical vein endothelium is altered in pathological pregnancies, including pregnancies with pre-established diabetes mellitus or in gestational diabetes. The mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs). Human endothelial cells from placenta microcirculation (hPMEC) express functional equilibrative nucleoside transporters 1 (hENT1) and 2 (hENT2) in culture. ENTs-mediated adenosine transport is regulated by insulin in human umbilical vein endothelium from normal or gestational diabetic (GD) pregnancies, but no information is available regarding the effect of this hormone in hPMEC. We propose to study the insulin effect in the expression of human equilibrative nucleoside transporters and adenosine transport in microvascular (hPMEC). Moreover, we propose to evaluate putative envolved mechanism in the blood flow regulation in the fetus-placenta unity.