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在三乙烯诱导的免疫损伤中,MPTP控制mtDNA的释放并诱导内皮细胞PANoptosis

Haibo Xie1, Jingyi Zhao2, Jian Chen2

  • 1Department of Dermatology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, Anhui, China; Institute of Dermatology, Anhui Medical University, Hefei 230032, Anhui, China.

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三乙烯 (TCE) 暴露会通过内皮细胞的PANoptosis引发损伤. 瘤死因α (TNF-α) 和干扰素γ (IFN-γ) 诱导线粒体损伤,导致干扰素调节因子1 (IRF1) 和Z核酸结合蛋白1 (ZBP1) 的激活.

关键词:
内皮细胞线粒体DNA线粒体透性过渡孔泛光症三乙烯

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科学领域:

  • * 分子和细胞生物学
  • * 免疫学
  • * 脏病学

背景情况:

  • * 内皮细胞损伤是损伤的一个关键因素.
  • * 三乙烯 (TCE) 暴露可能导致免疫损伤.
  • * 干扰素调节因子1 (IRF1) 介导的细胞衰竭与TCE诱导的损伤有关,但确切的机制尚不清楚.

研究的目的:

  • * 阐明IRF1在 EC中调节PAN的机制.
  • * 研究TNF-α和IFN-γ在TCE诱导的内皮细胞损伤和PANoptosis中的作用.
  • * 确定缓解TCE引起的损伤的治疗点.

主要方法:

  • * 使用TCE敏感的小鼠模型,在人静脉内皮细胞 (HUVEC) 的体外实验,以及人口研究.
  • 在因三乙烯 (OMDT) 引起的职业药物类皮肤炎患者中分析了TNF-α和IFN-γ的血清水平.
  • 使用环素A (CsA) 抑制线粒体透过渡孔 (mPTP) 开放,并评估下游分子事件.

主要成果:

  • * 血清TNF-α和IFN-γ水平与OMDT患者的和EC损伤相关.
  • * 结合TNF-α和IFN-γ促进了mPTP的开放,导致线粒体活性氧物种 (mtROS) 和线粒体DNA (mtDNA) 的释放.
  • * CsA 治疗减少了 mtDNA 释放,抑制了 PANoptosis,并降低了 IRF1 和 Z-核酸结合蛋白 1 (ZBP1) 的表达.
  • *mtDNA的存在增强了内核IRF1转录,对ZBP1进行上调,该转录识别mtDNA并驱动PANoptosis.

结论:

  • * TNF-α和IFN-γ通过mPTP开放和随后的mtDNA释放诱导EC PANoptosis.
  • * 一个涉及mtDNA,IRF1和ZBP1的信号级联在TCE暴露中调解 EC PANoptosis.
  • * 针对mPTP开放或IRF1/ZBP1通路可能为TCE诱导的损伤提供治疗策略.