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ATP5J通过线粒体功能障碍调节微质激活,加剧脑内出血时的神经炎症

Naixin Ren¹, Hutao Zhang¹, Tao Li¹

¹Department of Pathology, First Clinical Hospital, Harbin Medical University, Harbin, China.

Frontiers in immunology

|December 30, 2024

概括

线粒体ATP合成酶合因子6 (ATP5J) 通过损害微质功能,驱动脑出血后的神经炎症. 抑制ATP5J可能会防止二次脑损伤,并提供治疗点.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

微质介导的神经炎症是继脑内出血 (ICH) 之后的二次脑损伤 (SBI) 的关键因素.
线粒体在调节炎症和细胞功能方面发挥着至关重要的作用,ATP合成酶合因子6 (ATP5J) 参与了各种病理过程.
在ICH后的微质激活和神经炎症中,ATP5J的特定作用仍然在很大程度上未知.

研究的目的:

在ICH的背景下,研究ATP5J对微质激活和随后的神经炎症的影响.
阐明ATP5J影响微质功能和ICH后的神经炎症的潜在分子机制.

主要方法:

在ICH小鼠模型中利用了ATP5J的AAV9-介导基因操纵 (过度表达和淘汰).
采用了体外模型,使用用氧血球蛋白 (OxyHb) 刺激的BV2细胞来模拟ICH条件.
评估神经行为缺陷,血脑屏障完整性,脑水含量,微质激活,神经元亡和线粒体功能 (包括Drp1,Fis1,ROS和电子运输链活动).

主要成果:

在ICH后,ATP5J在微质上升调节,其过度表达加剧了SBI,神经行为缺陷和血脑屏障破坏.
ATP5J敲击改善了ICH诱导的损伤,减少了微质激活,神经元亡和炎症反应.
在机械上,ATP5J沉默逆转了线粒体功能障碍,减少了反应性氧物种的产生,并恢复了线粒体形态和微质中的电子运输链活动.

结论:

ATP5J是ICH后微质功能转换的关键调节者,主要通过调节线粒体功能障碍和新陈代谢.
向ATP5J可以减轻神经炎症,并预防脑内出血后的二次脑损伤.
ATP5J代表了一种潜在的分子和治疗点,用于缓解ICH中的神经炎症.

关键词:

在 ATP5J 中,脑内出血脑内出血微质细胞中的微质细胞线粒体重编程是什么意思二次性脑损伤是什么意思

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