Abstract
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.
Highlights
The present study aimed to investigate umbilical cord (UC) leptin receptor (LEPR) levels in PE and to examine the direct effect of leptin on IL-8 production by human endometrial endothelial cells (HEECs) and human umbilical vein endothelial cells (HUVECs), to describe the function of leptin in PE
LEPR immunostaining was detected in the cytoplasm and nucleus of the UC artery and vein endothelial cells
LEPR histologic score (HSCORE) were significantly different between the control vs. PE specimens in the sectioned UC arterial endothelial cells [mean ± standard error of the mean (SEM): 67.9±8.868 vs. 127.6±23.1; p=0.011, respectively] (Figure 1) and UC vein endothelial cells
Summary
In the pathogenesis of PE, activation of neutrophils, monocytes, and natural killer cells initiate inflammation, resulting in endothelial destruction in the pathogenesis of PE[4]. Mounting data imply that leptin is a novel proinflammatory adipocyte-originated element that manages the cytokine pathway by connecting the immune and inflammatory system[7,8]. IL-8 has been reported to activate chemotactic migration, proliferation, and survival of vascular endothelial cells; induce the expressions of vascular endothelial growth factor (VEGF) and VEGF receptor[10], and regulate pathologic angiogenesis[11]. Increased IL-8 levels have been described in various inflammatory diseases[13] Many inflammatory cells, such as monocytes, lymphocytes, and mast cells, release IL-8 that is accumulated inside endothelial cells. Neutrophil activation results in progressive damage to endothelial cells[16]. The present study aimed to investigate umbilical cord (UC) leptin receptor (LEPR) levels in PE and to examine the direct effect of leptin on IL-8 production by human endometrial endothelial cells (HEECs) and human umbilical vein endothelial cells (HUVECs), to describe the function of leptin in PE
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