The Experts below are selected from a list of 1854 Experts worldwide ranked by ideXlab platform
Li Zou - One of the best experts on this subject based on the ideXlab platform.
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ephB4 regulates human trophoblast cell line htr 8 svneo function implications for the role of ephB4 in preeclampsia
Biology of Reproduction, 2016Co-Authors: Xiaoping Liu, Xiaoxia Liu, Weifang Liu, Yanfang Zheng, Minglian Luo, Yin Zhao, Li ZouAbstract:Successful pregnancy depends on well-regulated extravillous trophoblast (EVT) invasion into the uterine decidua and moderate uterine spiral artery remodeling. Ephrin Receptor B4 (EPHB4) is a membrane-anchored Receptor tyrosine kinase that plays an important role in various cellular functions in human normal tissue and tumors. Reportedly, EPHB4 plays important roles during placentation. Still, there is no investigation of EPHB4 modulating trophoblast function. In our study, term placentas of preeclamptic pregnancies showed a significantly increased EPHB4 expression compared to those of uncomplicated pregnancies (n = 15). Exogenous up-regulation of EPHB4 in HTR-8/SVneo cells was performed to investigate the effects of EPHB4 on cell biological behavior. The results showed that EPHB4 enhancement reduced cell proliferation and promoted trophoblast apoptosis; and inhibited cell migration, invasion, and endothelial replacement. Associated factors, such as matrix metalloproteinases, vascular endothelial growth factor, placental growth factor, and soluble Fms-like tyrosine kinase 1 were examined at transcriptional level. Furthermore, cell functional results were confirmed in a placenta-decidua coculture system, showing poor vascular remodeling. Additionally, we detected possible down-stream PI3K-Akt signal pathway involved in EPHB4-mediated function of HTR-8/SVneo cells. Our study demonstrates that EPHB4 overexpression may contribute to trophoblasts dysfunction and impair maternal artery remodeling, as is associated with the pathogenesis of preeclampsia.
Xiaoping Liu - One of the best experts on this subject based on the ideXlab platform.
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ephB4 regulates human trophoblast cell line htr 8 svneo function implications for the role of ephB4 in preeclampsia
Biology of Reproduction, 2016Co-Authors: Xiaoping Liu, Xiaoxia Liu, Weifang Liu, Yanfang Zheng, Minglian Luo, Yin Zhao, Li ZouAbstract:Successful pregnancy depends on well-regulated extravillous trophoblast (EVT) invasion into the uterine decidua and moderate uterine spiral artery remodeling. Ephrin Receptor B4 (EPHB4) is a membrane-anchored Receptor tyrosine kinase that plays an important role in various cellular functions in human normal tissue and tumors. Reportedly, EPHB4 plays important roles during placentation. Still, there is no investigation of EPHB4 modulating trophoblast function. In our study, term placentas of preeclamptic pregnancies showed a significantly increased EPHB4 expression compared to those of uncomplicated pregnancies (n = 15). Exogenous up-regulation of EPHB4 in HTR-8/SVneo cells was performed to investigate the effects of EPHB4 on cell biological behavior. The results showed that EPHB4 enhancement reduced cell proliferation and promoted trophoblast apoptosis; and inhibited cell migration, invasion, and endothelial replacement. Associated factors, such as matrix metalloproteinases, vascular endothelial growth factor, placental growth factor, and soluble Fms-like tyrosine kinase 1 were examined at transcriptional level. Furthermore, cell functional results were confirmed in a placenta-decidua coculture system, showing poor vascular remodeling. Additionally, we detected possible down-stream PI3K-Akt signal pathway involved in EPHB4-mediated function of HTR-8/SVneo cells. Our study demonstrates that EPHB4 overexpression may contribute to trophoblasts dysfunction and impair maternal artery remodeling, as is associated with the pathogenesis of preeclampsia.
Yaqin Wang - One of the best experts on this subject based on the ideXlab platform.
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microrna 652 3p promotes the proliferation and invasion of the trophoblast htr 8 svneo cell line by targeting homeobox a9 to modulate the expression of Ephrin Receptor B4
Clinical and Experimental Pharmacology and Physiology, 2019Co-Authors: Ziyun Shi, Bo Liu, Feifei Liu, Xiaohua Yuan, Yaqin WangAbstract:MicroRNAs (miRNAs) are emerging as novel modulators in the pathogenesis of preeclampsia (PE). Multiple miRNAs have been shown to regulate the proliferation and invasion of trophoblast cells, which play a critical role in successful pregnancies. miR-652-3p has been identified as a novel disease-associated miRNA that is dysregulated in various pathological processes. However, whether miR-652-3p is dysregulated in PE and regulates the cellular function of trophoblast cells remains unknown. In the present study, we aimed to investigate the expression pattern of miR-652-3p in PE and explore its potential function in trophoblast cells. Herein, we found that miR-652-3p expression was significantly decreased in the placental tissues of pregnant women with PE. Cellular function experiments showed that overexpression of miR-652-3p promoted the viability, proliferation, and invasion of trophoblast cells in vitro. By contrast, inhibition of miR-652-3p had the opposite effect. Bioinformatics analysis predicted that homeobox A9 (HOXA9), a crucial regulator of trophoblast cell function, was a potential target gene of miR-652-3p. A luciferase reporter assay confirmed that miR-652-3p directly interacted with the 3'-untranslated region of HOXA9. Moreover, miR-652-3p was shown to negatively regulate the expression of HOXA9 and Ephrin Receptor B4 (EphB4) in trophoblast cells. Notably, overexpression of HOXA9 or EphB4 significantly reversed the regulatory effect of miR-652-3p on proliferation and invasion of trophoblast cells. Taken together, our findings demonstrate that miR-652-3p regulates the proliferation and invasion of trophoblast cells, possibly through targeting HOXA9 and modulating EphB4 expression.
Jin Yan - One of the best experts on this subject based on the ideXlab platform.
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microrna 454 is involved in regulating trophoblast cell proliferation apoptosis and invasion in preeclampsia by modulating the expression of Ephrin Receptor B4
Biomedicine & Pharmacotherapy, 2018Co-Authors: Furong Wang, Jin YanAbstract:Preeclampsia (PE) is a pregnancy-specific disorder representing a major cause for maternal and perinatal morbidity and mortality. The dysfunction of trophoblast cells plays an important role in the pathogenesis of PE. In recent years, microRNAs (miRNAs) have been suggested to play an important role in regulating trophoblast cell biological functions involved in the pathogenesis of PE. Accumulating evidence has showed that miR-454 plays an important role in regulating cell functions. However, whether miR-454 is involved in regulating cell functions of trophoblast cells during PE remains unclear. In this study, we found that miR-454 expression was significantly downregulated in placental tissues from PE patients. in vitro experiments showed that miR-454 overexpression significantly increased proliferation, inhibited apoptosis, and promoted invasion of trophoblast cells, whereas miR-454 inhibition markedly suppressed proliferation, increased apoptosis, and inhibited invasion of trophoblast cells. Interestingly, bioinformatics analysis predicted that Ephrin Receptor B4 (EPHB4), an important gene for regulating trophoblast cell function in PE, was a potential target gene of miR-454. Dual-luciferase reporter assay showed that miR-454 directly targeted the 3'-untranslated region of EPHB4. Real-time quantitative polymerase chain reaction and Western blot analysis demonstrated that miR-454 negatively regulated EPHB4 expression in trophoblast cells. Moreover, miR-454 expression was found inversely correlated with EPHB4 expression in placental tissues from PE patients. Importantly, EPHB4 overexpression partially reversed the promotion effect of miR-454 overexpression on trophoblast cell proliferation and invasion. Taken together, these findings demonstrate that miR-454 promotes the proliferation and invasion of trophoblast cells by inhibiting EPHB4 expression, and the decreased miR-454 expression may contribute to PE by promoting EPHB4 expression. Our study provides novel insights into understanding the molecular pathogenesis of PE.
Yin Zhao - One of the best experts on this subject based on the ideXlab platform.
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ephB4 regulates human trophoblast cell line htr 8 svneo function implications for the role of ephB4 in preeclampsia
Biology of Reproduction, 2016Co-Authors: Xiaoping Liu, Xiaoxia Liu, Weifang Liu, Yanfang Zheng, Minglian Luo, Yin Zhao, Li ZouAbstract:Successful pregnancy depends on well-regulated extravillous trophoblast (EVT) invasion into the uterine decidua and moderate uterine spiral artery remodeling. Ephrin Receptor B4 (EPHB4) is a membrane-anchored Receptor tyrosine kinase that plays an important role in various cellular functions in human normal tissue and tumors. Reportedly, EPHB4 plays important roles during placentation. Still, there is no investigation of EPHB4 modulating trophoblast function. In our study, term placentas of preeclamptic pregnancies showed a significantly increased EPHB4 expression compared to those of uncomplicated pregnancies (n = 15). Exogenous up-regulation of EPHB4 in HTR-8/SVneo cells was performed to investigate the effects of EPHB4 on cell biological behavior. The results showed that EPHB4 enhancement reduced cell proliferation and promoted trophoblast apoptosis; and inhibited cell migration, invasion, and endothelial replacement. Associated factors, such as matrix metalloproteinases, vascular endothelial growth factor, placental growth factor, and soluble Fms-like tyrosine kinase 1 were examined at transcriptional level. Furthermore, cell functional results were confirmed in a placenta-decidua coculture system, showing poor vascular remodeling. Additionally, we detected possible down-stream PI3K-Akt signal pathway involved in EPHB4-mediated function of HTR-8/SVneo cells. Our study demonstrates that EPHB4 overexpression may contribute to trophoblasts dysfunction and impair maternal artery remodeling, as is associated with the pathogenesis of preeclampsia.