A&R:坏死性凋亡对特发性炎症性肌病肌纤维死亡的作用

2022-06-21 MedSci原创 MedSci原创

过度激活的坏死性凋亡会导致特发性炎症性肌病(IIMs)的肌肉损伤,并表明坏死性凋亡抑制剂可能代表治疗IIM的新治疗靶点。

目的肌纤维坏死是特发性炎症性肌病(IIMs)的一个重要病理特征,其分子机制在很大程度上是未知的。坏死性凋亡是最近发现的一种不依赖于半胱天冬酶的受调节的坏死细胞死亡形式,主要由受体相互作用蛋白1 (RIP1)RIP3和混合谱系激酶域样(MLK​​L)介导。坏死性凋亡的激活可能具有重要的生物学后果。本研究的目的是调查坏死性凋亡在IIM肌肉损伤中的作用。

方法进行蛋白质印迹和免疫组织化学分析检查26IIM患者和4名健康对照中受体相互作用蛋白3 (RIP-3)MLK​​L蛋白的表达,以及坏死性凋亡相关损伤-相关分子模式分子。肿瘤坏死因子(TNF)用于刺激培养的C2C12成肌细胞,并在体外研究坏死性凋亡参与C2C12细胞的细胞死亡。

结果与健康对照组相比,IIM 患者肌肉组织中RIP-3MLKL蛋白及其磷酸化形式的表达显著增加RIP-3MLKL蛋白的表达水平与IIM患者肌肉损伤的严重程度相关。在IIM患者的肌肉活检组织中观察到MLKL与高迁移率组框染色体蛋白1在坏死性肌纤维中的显著共定位。TNF和泛半胱天冬酶抑制剂Z-VAD刺激C2C12成肌细胞导致坏死性凋亡过度激活并显著增加坏死细胞死亡。用necrostatin-1抑制坏死性凋亡或敲低MLKL表达的策略成功地阻止了C2C12细胞的坏死性凋亡诱导的细胞死亡。

结论这些发现表明,过度激活的坏死性凋亡会导致IIM的肌肉损伤,并表明坏死性凋亡抑制剂可能代表治疗IIM的新治疗靶点。

出处:Peng, Q.-L., Zhang, Y.-M., Liu, Y.-C., Liang, L., Li, W.-L., Tian, X.-L., Zhang, L., Yang, H.-X., Lu, X. and Wang, G.-C. (2022), Contribution of Necroptosis to Myofiber Death in Idiopathic Inflammatory Myopathies. Arthritis Rheumatol, 74: 1048-1058. https://doi.org/10.1002/art.42071

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    2022-12-06 okhuali
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    2022-06-21 millore
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