Nat Commun: 增加线粒体自噬可以保护糖皮质激素诱导的神经损伤

2021-01-21 haibei MedSci原创

最近,研究人员在Nature Communications发文,其研究了糖皮质激素在海马神经元、SH-SY5Y细胞和ICR小鼠的线粒体自噬抑制和后续突触缺陷中的作用。

压力诱导的糖皮质激素水平的增加是神经退行性疾病,如阿尔茨海默病(AD)的主要病因,其也会引发线粒体损伤。在正常的神经元中,受损的线粒体进行不对称的裂变,并被自噬途径清除,返回到细胞体在溶酶体中降解或在远端轴突被清除。这个过程被称为线粒体自噬,其可以帮助保持适当数量的健康线粒体,特别是在突触。

高浓度的糖皮质激素可以导致神经元中功能障碍的线粒体的积累。此外,肾上腺素,另一个压力诱导的因素,可以抑制自噬,这可能促进了线粒体功能障碍和神经退行性疾病,如AD。

如果不能消除受损的线粒体,在压力暴露的神经元中会诱导突触稳态异常,并最终导致神经退行性疾病。

最近,研究人员在Nature Communications发文,其研究了糖皮质激素在海马神经元、SH-SY5Y细胞和ICR小鼠的线粒体自噬抑制和后续突触缺陷中的作用。

首先,研究人员观察到糖皮质激素会降低突触密度和囊泡回收,这是由于线粒体自噬受到抑制导致的。

筛选数据显示,糖皮质激素下调BNIP3样(BNIP3L)/NIX,导致线粒体呼吸功能和突触密度降低

值得注意的是,研究人员还发现,糖皮质激素可引导糖皮质激素受体直接与PGC1α启动子结合,下调其表达和核转位。PGC1α的下调选择性地降低了NIX依赖的线粒体自噬。

与这些结果一致的是,用NIX增强剂预处理皮质酮暴露的小鼠可提升海马的线粒体自噬水平和突触密度,改善空间记忆任务的结果

总之,糖皮质激素通过下调NIX抑制线粒体自噬,NIX激活可能是恢复突触功能的潜在靶标。

 

原始出处:

Gee Euhn Choi et al. BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse defects. Nature Communications (2021). 

 

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    2021-08-28 liuli5079
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    2021-03-17 liye789132251
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    2021-01-23 易水河

    线粒体细胞的动力工厂

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