Is there any relationship between adipocytokines and angiogenesis factors to address endothelial dysfunction and platelet aggregation in untreated patients with preeclampsia?

Güngör, Zeynep; Ekmekçi, Hakan; Tüten, Abdullah; Toprak, S.; Ayaz, Gülsel; Çalışkan, Oktay; Sönmez, Hüseyin; Madazli, Rıza; Donma, Orkide; Kuçur, Mine; Ulutin, Turgut; Ekmekçi, Özlem Balcı

doi:10.1007/s00404-017-4461-2

Cited by 12 publications

(14 citation statements)

References 50 publications

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“…For example, leptin levels were found raised in the GD group of pregnant women, even when adjusting for confounders [86]. Higher serum leptin levels in pregnant women with PE have also been documented [91,92], and there is an association between higher leptin expression and intrauterine growth restriction (IUGR) [93,94]. To date, a few studies have shown a relationship between BPA and leptin.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation

Greca

Kyrou

Pink

et al. 2020

JCM

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Background: Endocrine-disrupting chemicals (EDCs) are environmental chemicals/toxicants that humans are exposed to, interfering with the action of multiple hormones. Bisphenol A (BPA) is classified as an EDC with xenoestrogenic activity with potentially adverse effects in reproduction. Currently, a significant knowledge gap remains regarding the complete spectrum of BPA-induced effects on the human placenta. As such, the present study examined the effects of physiologically relevant doses of BPA in vitro. Methods: qRT-PCR, Western blotting, immunofluorescence, ELISA, microarray analyses, and bioinformatics have been employed to study the effects of BPA using nonsyncytialised (non-ST) and syncytialised (ST) BeWo cells. Results: Treatment with 3 nM BPA led to an increase in cell number and altered the phosphorylation status of p38, an effect mediated primarily via the membrane-bound estrogen receptor (GPR30). Nonbiased microarray analysis identified 1195 and 477 genes that were differentially regulated in non-ST BeWo cells, whereas in ST BeWo cells, 309 and 158 genes had altered expression when treated with 3 and 10 nM, respectively. Enriched pathway analyses in non-ST BeWo identified a leptin and insulin overlap (3 nM), methylation pathways (10 nM), and differentiation of white and brown adipocytes (common). In the ST model, most significantly enriched were the nuclear factor erythroid 2-related factor 2 (NRF2) pathway (3 nM) and mir-124 predicted interactions with cell cycle and differentiation (10 nM). Conclusion: Collectively, our data offer a new insight regarding BPA effects at the placental level, and provide a potential link with metabolic changes that can have an impact on the developing fetus.

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Section: Discussionmentioning

confidence: 99%

Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation

Greca

Kyrou

Pink

et al. 2020

JCM

View full text Add to dashboard Cite

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“…Several studies illustrated the potential role of cytokines, chemokines, and their receptors in the development and progression of PE ( 19 , 20 , 21 ) . Pregnancy complications associated with PE are major causes of materno-fetal morbidity and mortality, but their pathogenesis remains unclear ( 22 ) .…”

Section: Discussionmentioning

confidence: 99%

“…Leptin is produced by cytotrophoblasts and syncytiotrophoblasts in the human placenta and adipose tissue, which is then secreted into the circulation, where it exerts its effects via interaction with the LEPR. The effect of leptin on endothelial cells has attracted particular attention ( 20 , 26 ) . LEPRs are expressed in many normal tissues, but also in pathologic tissues generally associated with obesity and abnormal energy balance ( 27 ) .…”

Section: Discussionmentioning

confidence: 99%

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

Arlıer¹

2017

tjod

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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.

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“…Its level increases in plasma as a result of endothelial damage. vWF increases platelet adhesion to subendothelial layer and contributes to thrombus formation [40,41].…”

Section: Endothelial Dysfunction and Cardiovascular Diseasesmentioning

confidence: 99%

Vascular Inflammation and Genetic Predisposition as Risk Factors for Cardiovascular Diseases

Güngör¹

2018

Cholesterol - Good, Bad and the Heart

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Atherosclerosis previously defined as an obstructive disease leads to fatty deposits in the arterial wall. Nowadays, according to the best of our knowledge, specific cells, molecular mechanisms, and genes play crucial roles in the pathogenesis of the disease. Inflammatory reaction contributes to atherosclerotic lesion formation, since fatty streak leads to a plaque erosion or rupture. Experimental and clinical studies have shown that besides well-known risk factors, such as smoking, hypertension, diabetes, and dyslipidemia, genetic variations in certain locuses affect the disease burden. A common genetic variability at the apoE locus has been shown to be associated with a risk for cardiovascular disease. In many studies, a higher cardiovascular risk has been associated with the presence of the apo ε4 allele, whereas the apo ε2 allele has been protective. Recent studies stated that pro-inflammatory cytokines increase the binding of low-density lipoprotein (LDL) to endothelium and smooth muscle cells, so inflammatory response solely increases lipoprotein accumulation within the vessel wall. As a conclusion, cholesterol accumulation leads to atherosclerotic plaque via several mechanisms. Genetic predisposition and inflammatory process may affect disease severity.

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Is there any relationship between adipocytokines and angiogenesis factors to address endothelial dysfunction and platelet aggregation in untreated patients with preeclampsia?

Cited by 12 publications

References 50 publications

Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation

Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation

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

Vascular Inflammation and Genetic Predisposition as Risk Factors for Cardiovascular Diseases

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