Chemerin promotes the viability and migration of human placental microvascular endothelial cells and activates MAPK/AKT signaling

In preeclampsia, maternal serum chemerin level is significantly increased and associated with dyslipidemia. However, the mechanism by which chemerin contributes to the pathogenesis of preeclampsia remains elusive. This study aimed to investigate the effect of chemerin on placental microvascular generation using human placental microvascular endothelial cells (HPMECs) as the experimental model. HPMECs were isolated and cultured and then treated with chemerin at different concentrations (0.1, 0.3, 1.0, 3.0 and 10.0 ng/ml). The viability, migration and tube formation of HPMECs were evaluated. The expression of chemerin receptor ChemR23 and the activation of MAPK/AKT pathway were analyzed by Western blot analysis. HPMECs isolated were positive for vWf and CD31 staining. Chemerin enhanced the viability, migration and tube formation of HPMECs, and significantly increased the expression of ChemR23. In addition, chemerin activated ERK1/2, p38MAPK and Akt pathways. In conclusion, chemerin promotes the formation of blood vessels in human placenta and activates Akt and MAPKs pathways, which may be involved in the occurrence and progression of preeclampsia.