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Inconformity of CXCL3 Plasma Level and Placenta Expression in Preeclampsia and Its Effect on Trophoblast Viability and Invasion

机译:子痫前期CXCL3血浆水平和胎盘表达的不符合及其对滋养细胞活力和侵袭的影响

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摘要

As a member of the chemokine family, CXCL3 was previously known to participate in many pathophysiological events. However, whether CXCL3 stimulates trophoblast invasion as a key process of preeclampsia pathogenesis remains largely unknown. Therefore, the aim of this study was to investigate this hypothesis and determine the effect of CXCL3 on the first trimester trophoblast. Seventy gravidas were included in this study. ELISA was used to detect CXCL3 plasma levels on preeclampsia and normal pregnant groups. CXCL3 protein and mRNA levels were detected via Western blot and real-time quantitative PCR analysis after immunolocalized in human placenta. Moreover, the CXCL3 function in HTR-8/Svneo was analyzed via WST-1 assay, flow cytometry and invasion test. The plasma CXCL3 level in preeclampsia was significantly higher than that in normal pregnancy. CXCL3 expression was observed in the cytoplasm of placental trophoblasts and vascular endothelium in all groups without significant difference between maternal and fetal sides. In addition, placenta CXCL3 expression in severe preeclampsia was significantly lower than those in normal and mild PE groups. Moreover, exogenous CXCL3 can promote the proliferation and invasion of HTR-8/Svneo; however, its effect on apoptosis remains unclear. In summary, a significant abnormality of plasma CXCL3 level and placental CXCL3 expression was discovered in severe preeclampsia; CXCL3 had a function in trophoblast invasion, which indicated its participation in shallow implantation. Therefore CXCL3 might be involved in severe preeclampsia pathogenesis.
机译:作为趋化因子家族的成员,以前已知CXCL3参与许多病理生理事件。但是,CXCL3是否作为子痫前期发病机理的关键过程而刺激滋养细胞的入侵仍是未知之数。因此,本研究的目的是调查这一假设并确定CXCL3对早孕滋养细胞的影响。这项研究包括七十个孕妇。 ELISA用于检测先兆子痫和正常妊娠组的CXCL3血浆水平。免疫定位于人胎盘后,通过蛋白质印迹和实时定量PCR分析检测CXCL3蛋白和mRNA水平。此外,通过WST-1测定,流式细胞术和侵袭试验分析了CXCL3在HTR-8 / Svneo中的功能。子痫前期的血浆CXCL3水平显着高于正常妊娠。在所有组的胎盘滋养细胞和血管内皮细胞的细胞质中均观察到了CXCL3的表达,母体和胎儿侧之间均无显着差异。此外,严重子痫前期的胎盘CXCL3表达明显低于正常和轻度PE组。此外,外源CXCL3可以促进HTR-8 / Svneo的增殖和侵袭。然而,其对细胞凋亡的作用仍不清楚。总之,在严重子痫前期中发现血浆CXCL3水平和胎盘CXCL3表达有明显异常。 CXCL3具有滋养细胞入侵的功能,表明其参与了浅层植入。因此CXCL3可能参与了严重的子痫前期发病机制。

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