Chemerin plays a protective role by regulating human umbilical vein endothelial cell-induced nitric oxide signaling in preeclampsia.

The aim of this study was to determine chemerin levels in preeclampsia and to assess the effects of this anti-inflammatory factor on endothelial nitric oxide synthase (eNOS), nuclear factor (NF)-κB, and vascular cell adhesion molecule (VCAM) expression in human umbilical vein endothelial cells (HUVECs). Serum chemerin and eNOS levels were measured by enzyme-linked immunosorbent assays, while chemerin mRNA and protein levels were measured by fluorescent quantitative polymerase chain reaction and Western blotting, respectively. Nitric oxide (NO) concentrations were determined with a colorimetric method. Akt and eNOS phosphorylation were assessed by Western blotting. We also tested the effects of the phosphoinositide 3-kinase inhibitor LY294002 and the eNOS inhibitor L-NAME. NF-κB p65 and VCAM-1 phosphorylation were assessed by Western blotting to investigate the role of chemerin in tumor necrosis factor (TNF)-α-induced HUVEC injury. Serum chemerin levels were increased in preeclampsia, while eNOS was decreased. Chemerin mRNA and protein were both increased in placentae from patients with preeclampsia. Furthermore, chemerin serum level positively correlated with blood pressure, body mass index, and serum insulin and was negatively correlated with serum eNOS. Chemerin dose-dependently increased NO concentrations in supernatants. Chemerin can increase eNOS and Akt levels in HUVECs, and these results could be partly blocked by LY294002 and L-NAME. Chemerin significantly decreased TNF-α-induced NF-κB and VCAM-1 in HUVECs, and these changes were partly inhibited by LY294002 and L-NAME. Chemerin may play a protective role by regulating NO signaling. Future studies should assess the role of chemerin in preeclampsia and other vascular diseases.