CMPL research is focused on vascular dysfunction in diseases of pregnancy.

Human endothelial dysfunction is a common feature in diseases of pregnancy such as gestational diabetes (GD), pre-eclampsia (PE) and intrauterine growth restriction (IUGR).

Metabolic changes include altered synthesis of nitric oxide (NO), and altered membrane transport of L-arginine and adenosine in primary cultures of human umbilical vein (HUVEC, macrovascular) and placenta microvillous (hPMEC, microvascular) endothelial cells. These alterations are associated with modifications in the expression and activity of endothelial (eNOS) and inducible (iNOS) NO synthases, respectively, an effect maintained up to passage 5 in culture. Expression and activity of the human cationic amino acid transporter 1 (hCAT-1) and equilibrative nucleoside transporters 1 (hENT1) and hENT2, as well as the correspondingSLC7A1, SLC29A1andSLC29A2gene promoter activities, is exhibited by these cell types. Altered gene expression results from increased NO level, PKC, MAPK, hCHOP-C/EBP a and Sp1 transcription factors activation. Reduced ENTs-mediated adenosine transport in GD and PE is associated with stimulation of L-arginine/NO pathway. In addition, hENT2 activity seems to intend to restore the reduced adenosine transport in GD and PE . It is suggested that a common functional characteristic leading to changes in the bioavailability of adenosine is evidenced by human fetal micro and macrovascular endothelium in GD, PE and IUGR.