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首页> 外文期刊>Cell cycle >MicroRNA-138 improves LPS-induced trophoblast dysfunction through targeting RELA and NF-kappa B signaling
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MicroRNA-138 improves LPS-induced trophoblast dysfunction through targeting RELA and NF-kappa B signaling

机译：MicroRNA-138通过靶向Rela和NF-Kappa B信号来改善LPS诱导的滋养板功能障碍

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摘要

Preeclampsia is a pregnancy complication classified by new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. During preeclampsia, extra villous trophoblasts fail to adequately invade the myometrial spiral arteries, leading to incomplete and impaired vessel transformation and initiating or aggravating preeclampsia. Although NF-kappa B and proinflammatory cytokines have been reported to be related to trophoblast dysfunction, the underlying mechanism remains unclear. Herein, we demonstrated the miR-138/RELA axis modulating the migratory ability, and invasive ability of HTR-8/SVneo and JEG-3 cells, as well as the inflammatory factor levels in response to LPS stimulation. miR-138 expression was upregulated in preeclampsia placenta and LPS-stimulated HTR-8/SVneo and JEG-3 cell lines. miR-138 overexpression rescued the migratory and invasive ability of HTR-8/SVneo and JEG-3 cells inhibited by LPS stimulation, and decreased LPS-induced TNF-alpha and IL-6 levels. By binding the 3'-UTR of RELA, miR-138 negatively regulated p65 expression. The silencing of p65 also improved LPS-induced HTR-8/SVneo and JEG-3 cell dysfunction and TNF-alpha and IL-6 levels. More importantly, p65 overexpression partially reversed the functions of miR-138 overexpression upon both cells, indicating that miR-138 exerted its biological effects through targeting RELA. In conclusion, miR-138 improves LPS-induced inflammation and oxidative stress on trophoblasts through targeting RELA and affecting NF-kappa B signaling. The miR-138/RELA axis might be involved in preeclampsia pathogenesis, which requires further in vivo and clinical researches.
机译：先兆子痫是一种妊娠并发症，根据妊娠20周后新发的高血压和蛋白尿进行分类。在子痫前期，绒毛外滋养层未能充分侵入子宫肌层螺旋动脉，导致血管转化不完全和受损，并引发或加重子痫前期。尽管有报道称NF-κB和促炎细胞因子与滋养层功能障碍有关，但其潜在机制尚不清楚。在此，我们证明了miR-138/RELA轴调节HTR-8/SVneo和JEG-3细胞的迁移能力和侵袭能力，以及炎症因子水平对LPS刺激的反应。miR-138在先兆子痫胎盘和LPS刺激的HTR-8/SVneo和JEG-3细胞系中表达上调。miR-138的过度表达挽救了被LPS刺激抑制的HTR-8/SVneo和JEG-3细胞的迁移和侵袭能力，并降低了LPS诱导的TNF-α和IL-6水平。通过结合RELA的3'-UTR，miR-138负调控p65的表达。p65的沉默也改善了LPS诱导的HTR-8/SVneo和JEG-3细胞功能障碍以及TNF-α和IL-6水平。更重要的是，p65过度表达部分逆转了miR-138过度表达对两种细胞的功能，表明miR-138通过靶向RELA发挥其生物学效应。总之，miR-138通过靶向RELA和影响NF-κB信号传导改善LPS诱导的滋养层炎症和氧化应激。miR-138/RELA轴可能参与子痫前期的发病机制，这需要进一步的体内和临床研究。

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  • 来源
    《Cell cycle》 |2021年第6期|共14页
  • 作者

    Yin Ailan; Chen Qian; Zhong Mei; Jia Bei;

  • 作者单位

    Southern Med Univ Nanfang Hosp Dept Gynecol &

    Obstet Guangzhou Peoples R China;

    Southern Med Univ Nanfang Hosp Dept Gynecol &

    Obstet Guangzhou Peoples R China;

    Southern Med Univ Nanfang Hosp Dept Gynecol &

    Obstet Guangzhou Peoples R China;

    Southern Med Univ Nanfang Hosp Dept Gynecol &

    Obstet Guangzhou Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Preeclampsia (PE); inflammation; miR-138; p65 (RELA); trophoblast;

    机译：预口局部（PE）;炎症;miR-138;p65（rela）;滋养板;

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