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首页> 外文期刊>Cell and Tissue Research >Endoplasmic reticulum stress may activate NLRP3 inflammasomes via TXNIP in preeclampsia
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Endoplasmic reticulum stress may activate NLRP3 inflammasomes via TXNIP in preeclampsia

机译：内质网胁迫可以通过PETECLAMPSIA的TXNIP激活NLRP3炎症

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摘要

Preeclampsia (PE) development is often associated with placental immune and inflammatory dysregulation, as well as endoplasmic reticulum (ER) stress. However, the mechanisms linking ER stress and inflammatory dysregulation to PE have not been elucidated. It has been reported that thioredoxin-interacting protein (TXNIP), which can bind with and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, is a key point in immune regulation. Recent experimental evidence suggests that activated NLRP3 inflammasomes can activate interleukin-1 beta (IL-1 beta) production in the placenta of patients with PE. The objective of the current study was to explore if TXNIP plays a critical signaling role linking ER stress with NLRP3 inflammasome activation in PE. We hypothesized that ER stress would induce TXNIP production, which would bind with NLRP3 inflammasomes to activate IL-1 beta production. These cells showed a higher protein level of NLRP3 and IL-1 beta, as well as a higher enzymatic activity of caspase-1, indicating enhanced inflammatory dysregulation and ER stress. Cells transfected with TXNIP siRNA showed reduced NLRP3 inflammasome activation. Cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, showed a similar result. Outgrowth of the explant with TXNIP lentivirus in H/R or tunicamycin (inducers of ER stress) was also measured to verify our hypothesis. These findings demonstrated that TXNIP could influence inflammatory dysregulation by mediating ER stress and NLRP3 inflammasome activation in PE. This novel mechanism may further explain the inflammation observed at the maternal-fetal interface, which leads to placental dysfunction in a patient with PE.
机译：先兆子痫（PE）的发育通常与胎盘免疫和炎症性失调相关，以及内质网（ER）应激。然而，没有阐明将ER应激和炎症性失调的机制尚未得到阐明。据报道，可以将含有3（NLRP3）炎症的NLR家族吡林结构域与含有3（NLRP3）炎症的NLR家族吡林结构域的硫昔林相互作用蛋白（TXNIP）是免疫调节的关键点。最近的实验证据表明，活化的NLRP3炎性炎症可以在PE患者的胎盘中激活白细胞介素-1β（IL-1β）产生。目前研究的目的是探讨TXNIP在PE中与NLRP3炎症组合的关键信号传导作用。我们假设ER应激会诱导TXNIP生产，这将与NLRP3炎性炎症结合以激活IL-1β生产。这些细胞显示出较高的NLRP3和IL-1β的蛋白质水平，以及Caspase-1的更高酶活性，表明增强的炎性诱导剂和ER应力。用Txnip siRNA转染的细胞显示出降低的NLRP3炎症组活化。用4-苯基丁酸处理的细胞，ER应激的抑制剂，显示出类似的结果。还测量了在H / R或unicicamycin中的Txnip Lentivirus的外生病植体（ER应激的诱导剂）以验证我们的假设。这些发现证明，TXNIP通过在PE中介导ER应激和NLRP3炎症体活化来影响炎症性失衡。这种新机制可以进一步解释在母形界面处观察到的炎症，这导致患者在具有PE的患者中的胎盘功能障碍。

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  • 来源
    《Cell and Tissue Research》 |2020年第3期|共11页
  • 作者

    Yang Yong; Li Jianxin; Han Ting-Li; Zhou Xiaobo; Qi Hongbo; Baker Philip N.; Zhou Wei; Zhang Hua;

  • 作者单位

    Chngqing Hlth Ctr Women &

    Children Dept Obstet 120 Longshan Rd Chongqing 400021 Peoples R China;

    Chngqing Hlth Ctr Women &

    Children Dept Obstet 120 Longshan Rd Chongqing 400021 Peoples R China;

    Chongqing Med Univ Affiliated Hosp 1 Dept Obstet &

    Gynecol 1 Youyi Rd Chongqing 400016 Peoples;

    Chongqing Med Univ Affiliated Hosp 1 Dept Obstet &

    Gynecol 1 Youyi Rd Chongqing 400016 Peoples;

    Chongqing Med Univ Affiliated Hosp 1 Dept Obstet &

    Gynecol 1 Youyi Rd Chongqing 400016 Peoples;

    Chongqing Med Univ Canada China New Zealand Joint Lab Maternal &

    Fet 1 Yixueyuan Rd Chongqing;

    Chngqing Hlth Ctr Women &

    Children Dept Obstet 120 Longshan Rd Chongqing 400021 Peoples R China;

    Chongqing Med Univ Affiliated Hosp 1 Dept Obstet &

    Gynecol 1 Youyi Rd Chongqing 400016 Peoples;

  • 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; Endoplasmic reticulum (ER) stress; NLRP3; TXNIP;

    机译：预口兰（PE）;炎症;内质网（ER）应力;NLRP3;TXNIP;

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