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瘤坏死因子α诱导的内质网膜压力促进气道光滑肌肉细胞的增殖

Debanjali Dasgupta¹, Gary C Sieck¹

¹Department of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, MN 55905.

American journal of physiology. Lung cellular and molecular physiology

|January 6, 2026

概括

瘤亡因子α (TNFα) 触发了呼吸道平滑肌肉细胞通过内分泌网膜 (ER) 应激增殖. 这种途径激活环素B1,促进细胞生长,并且可以抑制以减少增殖.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
呼吸系统医学呼吸系统医学

背景情况:

支持炎症的细胞因子如TNFα刺激呼吸道光滑肌肉 (ASM) 细胞增殖.
TNFα诱导了内质网膜 (ER) 应激反应,涉及因诺醇,需要酶1α (IRE1α) 自酸化和X盒结合蛋白1 (XBP1) 拼接.
已知XBP1s可以通过转录激活循环素依赖激酶1和5 (CDK1和CDK5).

研究的目的:

调查pIRE1α^S724/XBP1s ER应激通路是否调解TNFα诱导的环素B1表达和ASM细胞增殖.
阐明ER应激通路在调节ASM细胞生长中的作用.

主要方法:

人类ASM (hASM) 细胞用TNFα,IRE1α抑制剂 (4μ8C) 或主导负XBP1突变 (δXBP1) 进行治疗.
分析了环素B1 (CCNB1) 和CDKs的基因表达.
使用CyQuant试验测量细胞增殖.
染色体免疫沉 (ChIP) 测定证实XBP1s与CCNB1促进体结合.

主要成果:

TNFα治疗诱导了pIRE1α^S724酸化和XBP1s在hASM细胞中的拼接.
发现XBP1s通过转录激活Cyclin B1 mRNA和蛋白质表达.
TNFα增加了环素B1的核定位,导致细胞增殖的增加.
抑制pIRE1α^S724/XBP1s通路减少了TNFα诱导的Cyclin B1和CDK表达和ASM细胞增殖.

结论:

皮尔1α^S724/XBP1s ER应激通路是TNFα诱导的环林B1表达的关键调解者.
这一途径在调节ASM细胞增殖方面发挥着重要作用.
针对 IRE1α/XBP1s 途径可能为涉及 ASM 过度扩散的疾病提供治疗策略.

关键词:

压力ERER压力ERER压力这就是TNFα.呼吸道炎症呼吸道炎症气道改造气道改造气道改造细胞的增殖细胞的增殖.

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