Circulating endothelial cell number and markers of endothelial dysfunction in previously preeclamptic women

Tuzcu, Zeyneb Başpehlivan; Aşıcıoğlu, Ebru; Sünbül, Murat; Özben, Beste; Arıkan, Hakkı; Koç, Mehmet

doi:10.1016/j.ajog.2015.06.043

Cited by 50 publications

(51 citation statements)

References 45 publications

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“…21,22 Similar to our results, a study on women with a history of preeclampsia reported higher sFlt1 level compared with controls. 23 VEGF plays a key role in EPC recruitment, enhancing mobilization and survival of EPCs, promoting vasculogenesis, and contributing to normal endothelial function. Moreover, it has been recently described that mice with PGC1-α deletion develop PPCM that is associated with an increased level of sFlt1 and insufficient upregulation of cardiac expression of VEGF blunted by sFlt1.…”

Section: Angiogenic Imbalance In Post-ppcm Women With LV Recoverymentioning

confidence: 99%

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Goland

Weinstein

Zalik

et al. 2016

Circ: Heart Failure

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Background-Recent studies suggest that angiogenic imbalance during pregnancy may lead to acute peripartum cardiomyopathy (PPCM). We propose that angiogenic imbalance and residual cardiac dysfunction may exist even after recovery from PPCM. Methods and Results-Twenty-nine women at least 12 months after presentation with PPCM, who exhibited recovery of left ventricular (LV) ejection fraction (≥50%), were included in the study (mean age 35±6 years, LV ejection fraction 61.0±3.9%). The number of circulating endothelial progenitor cells (EPCs) and plasma levels of proangiogenic vascular endothelial growth factor and of soluble vascular endothelial growth factor receptor Flt1 (sFlt1) Conclusions-Higher concentration of sFlt1 with concomitant decreased circulating endothelial progenitor cell levels along with inappropriate attenuated vascular endothelial growth factor levels may imply an angiogenic imbalance that exists even after recovery and may thus predispose to PPCM. In addition, tissue Doppler imaging and 2D strain were able to identify residual myocardial injury in post-PPCM women with apparent recovery of LV systolic function. Both angiogenic imbalance and residual myocardial injury may play an important role in the recurrence of LV dysfunction during subsequent pregnancies. (Circ Heart Fail. 2016;9:e003349.

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Section: Angiogenic Imbalance In Post-ppcm Women With LV Recoverymentioning

confidence: 99%

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Goland

Weinstein

Zalik

et al. 2016

Circ: Heart Failure

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“…Increased immunity activity in vessels and deterioration of protective barrier function due to damage to vascular endothelial cells is the most important effect on PE pathogenesis. [9][10][11] The immunological and molecular mechanisms that start this change in the veins and that are involved in this process have still not been understood in a clear manner, despite many studies being conducted. There are studies that have shown that glucocorticoids cause endothelial damage and function deterioration and those that use glucocorticoid in the treatment of endothelial damage.…”

Section: Discussionmentioning

confidence: 99%

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Arlıer

2017

EJMO

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Objectives:The objective of this study was to investigate the association between normal and preeclamptic glucocorticoid-induced leucine zipper (GILZ) levels in the placenta. Methods: Placental paraffin sections (5 μm) were obtained from gestational age-matched normal (n=9) and (PE) (n=9) pregnancies. Tissue sections were immunostained with rabbit monoclonal anti-human GILZ antibodies. Staining intensity of GILZ was evaluated with a histologic scoring (HSCORE) system. Parametric (t-test) and non-parametric tests (Mann-Whitney U) were used for statistical analysis, and a p value of <0.05 was considered significant. Results: Trophoblasts and endothelial cells were shown to be the source of GILZ release. Compared with the control, PE placental samples displayed significantly increased GILZ immunostaining HSCOREs in trophoblast cell nucleus (mean±SEM, 106.8±12.1 vs 167.9±14.9; p=0.006) and endothelial cells (95.0±8.1 vs 147.2±12.3; p=0.003). Conclusion: This study suggests that GILZ release by placental trophoblasts and endothelial cells may contribute to PE pathogenesis.

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“…Despite intensive efforts to delineate pathophysiology of pre-eclampsia, neither a specific cause nor a pathogenesis has been identified (1). One of the basic pathophysiologies of PE is the endothelial cell dysfunction as suggested by elevated of some nonspecific parameters (3). The main mechanism of the endothelial dysfunction is unclear.…”

Section: Introductionmentioning

confidence: 99%

Serum E-selectin in Preeclampsia: A Case â Control Study

Ayatollahi¹,

Khadem²,

Kianifar³

et al. 2018

J.JBTW

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Preeclampsia (PE) is an important disease in pregnancy, and is one of the causes of maternal morbidity, mortality and adverse neonatal outcomes. One of the basic pathophysiologies of preeclampsia is endothelial cell dysfunction as suggested by an elevated concentration of endothelin-selectin. The aim of this study was to compare the sera levels of endothelin-selectin (E-selectin) in normal and pre-eclamptic term pregnancy. This case-control study was followed on 80 patients admitted to the Departments of Obstetrics and Gynecology of the Ghaem and Emam Reza hospitals in Mashhad University of Medical Sciences. The Control group consisted of 40 normal term pregnant women (≥ 37 weeks) and the Case group was 40 term preeclamptic pregnant women. Participants were enrolled after approval by the ethics committee and received the informed consent. E-selectin concentration evaluated in two groups. The level of E-selectin was significantly in two groups. It was higher in sera of pre-eclamptic patients than the normal pregnancy (p=0.0001). Especially, it was significantly higher in severe pre-eclamptic patients (p<0.05). In conclusion, the found results showed that E-selectin was increased in term of PE that and may be useful for predicting the severity of pre-eclampsia.

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Circulating endothelial cell number and markers of endothelial dysfunction in previously preeclamptic women

Cited by 50 publications

References 45 publications

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Serum E-selectin in Preeclampsia: A Case â Control Study

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Circulating endothelial cell number and markers of endothelial dysfunction in previously preeclamptic women

Cited by 50 publications

References 45 publications

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Angiogenic Imbalance and Residual Myocardial Injury in Recovered Peripartum Cardiomyopathy Patients

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Serum E-selectin in Preeclampsia: A Case â Control Study

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Serum E-selectin in Preeclampsia: A Case â Control Study