Endothelial cell leptin receptors, leptin and interleukin-8 in the pathogenesis of preeclampsia: An in-vitro study

Objective Increased leptin hormone and leptin receptor may enhance the generation of proinflammatory cytokines by endothelial cells and lead to endothelial dysfunction. This study assessed the umbilical cord endothelial leptin receptor levels in preeclampsia and investigated the effect of leptin on endothelial interleukin-8 (IL-8) production. Materials and Methods The association between IL-8 levels with leptin stimulation was investigated in leptin-treated human endothelial cells. Endothelial cell leptin receptor levels were evaluated using immunohistochemistry staining, and endothelial IL-8 protein expression by Western blot analysis. Data are presented as mean ± standard error of the mean (SEM). Statistical significance was analyzed using Student's t-test or Mann-Whitney U test and one-way analysis of variance. Results Leptin receptor immunoreactivity increased significantly in umbilical cord venous and arterial endothelial cells in normal pregnancy (n=12) compared with preeclampsia (n=7) endothelial cells. The corresponding preeclampsia versus control histologic scores (mean ± SEM) were 67.9±8.8 vs. 127.6±23.1, (p=0.011) for the leptin receptor and 55.4±8,0 vs. 93.7±17.1 (p=0.035), respectively, for the vein endothelial cells. Leptin treatment significantly increased IL-8 protein levels (control vs. 100 and 1000 ng/mL, p=0.003). Conclusion The findings of increased umbilical cord endothelial leptin receptor levels in preeclampsia and increased endothelial IL-8 expression with exposure to higher leptin concentrations may indicate the contribution of leptin to endothelial dysfunction and increased neutrophil-endothelial interaction, which are significant pathophysiologic features of preeclampsia.