Hypomethylation of tissue factor pathway inhibitor 2 in human placenta of preeclampsia

Xiao, Xirong; Tao, Xiang; Wang, Yongxiang; Zhu, Lisha; Ye, Yunzhen; Liu, Haiyan; Zhou, Qiongjie; Li, Xiaotian; Xiong, Yan

doi:10.1016/j.thromres.2017.02.005

Cited by 13 publications

(13 citation statements)

References 42 publications

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“…For example, Zhou et al found that TFPI2 expression caused impairment of invasion and proliferation, and induced apoptosis in BeWo and JEG3 cells. Xiao et al have also reported overexpression of TFPI2 and aberrant promoter methylation status presented in PE placentas, suggesting that an epigenetic mechanism might result in the pathogenesis of PE. However, the role of TFPI2 in the pathogenesis of PE is still unknown.…”

Section: Discussionmentioning

confidence: 97%

MiR‐616‐3p modulates cell proliferation and migration through targeting tissue factor pathway inhibitor 2 in preeclampsia

Jiang

et al. 2018

Cell Proliferation

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Section: Discussionmentioning

confidence: 97%

MiR‐616‐3p modulates cell proliferation and migration through targeting tissue factor pathway inhibitor 2 in preeclampsia

Jiang

et al. 2018

Cell Proliferation

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“…Xu et al () indicated that MiR‐616‐3p upregulation stimulates cell proliferation and migration via targeting TFPI2 in PE. Xiao et al () reported that long noncoding RNA 00473 silences TFPI‐2 epigenetically by binding to lysine‐specific demethylase 1, promoting trophoblasts' invasion and migration, which are dysregulated in PE. High HIF‐1α and VEGF expression could be observed in placenta tissues of PE women (Ali et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…VEGF and hypoxia inducible factor (HIF)‐1α are involved in the pathophysiology of PE, and the HIF1α‐VEGF axis participates in the regulation of tight junction that sustains normal placental barrier integrity (Ali, Salih, Elhassan, Mohmmed, & Adam, ; Zhang et al, ). Suppressor gene tissue factor pathway inhibitor 2 (TFPI‐2) is indicated to be aberrantly expressed in the placenta of PE and might contribute to the pathogenesis of PE (Xiao et al, ), meanwhile is supposed to be potential therapeutic target of PE (Xu et al, ).…”

Section: Introductionmentioning

confidence: 99%

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

Zheng

Huang

et al. 2019

Drug Development Research

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Preeclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality with few safe, effective, and minimally invasive therapeutics. Inflammation, oxidative stress, and angiogenic imbalance have been reported to contribute to PE pathogenesis. Vitexin (VI) possesses various pharmacological activities including the potent regulation of the above biological processes in different conditions. This study aims to investigate whether VI has therapeutic potential to PE and the underlying mechanisms. Sprague–Dawley pregnant rats pretreated with or without VI were fed with l‐NAME‐containing water to induce experimental PE. Results showed that VI decreased high systolic blood pressure and urinary protein in PE rats time‐ and dose‐dependently. Meanwhile, VI of higher dosage (45, 60 mg/kg) corrected abnormal pregnancy outcomes, including low pup weight and low pups/placenta ratio. In addition, VI of high dosage (60 mg/kg) decreased sFlt‐1, increased PlGF and alleviated oxidative stress both in blood and placental samples compared with nontreated PE group. Furthermore, VI alleviated placental TFPI‐2, HIF 1α, and VEGF in PE rats. In short, the present study suggests that the inhibition of placental TFPI‐2 and HIF‐1α/VEGF might be one of the potential mechanisms underlying the protective effects of VI to experimental PE induced by l‐NAME.

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“…Studies have shown that the TFPI2 promoter contains some of the CpG islands participating in transcriptional silencing [ [31] , [32] , [33] ]. To determine whether PARP1 mediates hyperglycemia-induced TFPI2 promoter DNA methylation thus decreasing TFPI2 activity, the methylation levels of CpG islands in the TFPI2 promoter were examined using the MassARRAY assay (Sequenom).…”

Section: Resultsmentioning

confidence: 99%

PARP1 deficiency protects against hyperglycemia-induced neointimal hyperplasia by upregulating TFPI2 activity in diabetic mice

et al. 2021

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Diabetes mellitus (DM) promotes neointimal hyperplasia, characterized by dysregulated proliferation and accumulation of vascular smooth muscle cells (VSMCs), leading to occlusive disorders, such as atherosclerosis and stenosis. Poly (ADP-ribose) polymerase 1 (PARP1), reported as a crucial mediator in tumor proliferation and transformation, has a pivotal role in DM. Nonetheless, the function and potential mechanism of PARP1 in diabetic neointimal hyperplasia remain unclear. In this study, we constructed PARP1 conventional knockout (PARP1 −/− ) mice, and ligation of the left common carotid artery was performed to induce neointimal hyperplasia in Type I diabetes mellitus (T1DM) mouse models. PARP1 expression in the aorta arteries of T1DM mice increased significantly and genetic deletion of PARP1 showed an inhibitory effect on the neointimal hyperplasia. Furthermore, our results revealed that PARP1 enhanced diabetic neointimal hyperplasia via downregulating tissue factor pathway inhibitor (TFPI2), a suppressor of vascular smooth muscle cell proliferation and migration, in which PARP1 acts as a negative transcription factor augmenting TFPI2 promoter DNA methylation. In conclusion, these results suggested that PARP1 accelerates the process of hyperglycemia-induced neointimal hyperplasia via promoting VSMCs proliferation and migration in a TFPI2 dependent manner.

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Hypomethylation of tissue factor pathway inhibitor 2 in human placenta of preeclampsia

Abstract: Over-expression of TFPI-2 and aberrant promoter mythylation status presented in the PE placentas, suggesting that epigenetic mechanism might contribute to the pathogenesis of PE.

Cited by 13 publications

References 42 publications

MiR‐616‐3p modulates cell proliferation and migration through targeting tissue factor pathway inhibitor 2 in preeclampsia

MiR‐616‐3p modulates cell proliferation and migration through targeting tissue factor pathway inhibitor 2 in preeclampsia

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

PARP1 deficiency protects against hyperglycemia-induced neointimal hyperplasia by upregulating TFPI2 activity in diabetic mice

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