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首页> 外文期刊>Journal of cellular physiology. >Proinflammation effect of Mst1 promotes BV-2 cell death via augmenting Drp1-mediated mitochondrial fragmentation and activating the JNK pathway
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Proinflammation effect of Mst1 promotes BV-2 cell death via augmenting Drp1-mediated mitochondrial fragmentation and activating the JNK pathway

机译：Proinflammation Mst1促进BV-2细胞的影响通过增加Drp1-mediated线粒体死亡分裂和激活物途径

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摘要

Inflammation has been increasingly studied as part of the pathophysiology of neurodegenerative diseases. Mammalian Ste20-like kinase 1 (Mst1), a key factor of the Hippo pathway, is connected to cell death. Unfortunately, little study has been performed to detect the impact of Mstl in neuroninflammation. The results indicated that Mstl expression was upregulated because of LPS treatment. However, the loss of Mstl sustained BV-2 cell viability and promoted cell survival in the presence of LPS treatment. Molecular investigation assay demonstrated that Mstl deletion was followed by a drop in the levels of mitochondrial fission via repressing Drp1 expression. However, Drp1 adenovirus transfection reduced the protective impacts of Mstl knockdown on mitochondrial stress and neuronal dysfunction. Finally, our results illuminated that Mstl affected Drp1 content and mitochondrial fission in a JNK-dependent mechanism. Reactivation of the JNK axis inhibited Mstl knockdown-mediated neuronal protection and mitochondrial homeostasis. Altogether, our results indicated that Mstl upregulation and the activation of JNK-Drp1-mitochondrial fission pathway could be considered as the novel mechanism regulating the progression of neuroninflammation. This finding would pave a new road for the treatment of neurodegenerative diseases via modulating the Mst1-JNK-Drp1-mitochondrial fission axis.
机译：作为炎症已经得到越来越多的研究神经变性的病理生理学疾病。河马通路的关键因素,是连接细胞死亡。进行检测的影响Mstlneuroninflammation。因为有限合伙人Mstl表达调节治疗。BV-2细胞生存能力,促进了细胞的生存有限合伙人的待遇。调查分析表明,Mstl删除之后的水平下降线粒体通过压抑Drp1裂变表达式。减少了Mstl击倒保护的影响在线粒体应激和神经功能障碍。最后,我们的结果照亮,Mstl影响Drp1内容和线粒体分裂在一个JNK-dependent机制。物轴抑制Mstl knockdown-mediated神经保护和线粒体体内平衡。, Mstl upregulation和激活JNK-Drp1-mitochondrial裂变通路视为小说机制调节neuroninflammation的进展。铺一条新路治疗吗通过调节的神经退行性疾病Mst1-JNK-Drp1-mitochondrial裂变轴。

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