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蛋白质精氨酸甲基转移酶 8 调节缺氧应激后的线粒体生物能量和神经炎症。

Protein arginine methyltransferase 8 modulates mitochondrial bioenergetics and neuroinflammation after hypoxic stress.

机构信息

Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA, USA.

Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA, USA.

出版信息

J Neurochem. 2021 Nov;159(4):742-761. doi: 10.1111/jnc.15462. Epub 2021 Aug 25.

DOI:10.1111/jnc.15462
PMID:34216036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8595568/
Abstract

Protein arginine methyltransferases (PRMTs) are a family of enzymes involved in gene regulation and protein/histone modifications. PRMT8 is primarily expressed in the central nervous system, specifically within the cellular membrane and synaptic vesicles. Recently, PRMT8 has been described to play key roles in neuronal signaling such as a regulator of dendritic arborization, synaptic function and maturation, and neuronal differentiation and plasticity. Here, we examined the role of PRMT8 in response to hypoxia-induced stress in brain metabolism. Our results from liquid chromatography mass spectrometry, mitochondrial oxygen consumption rate, and protein analyses indicate that PRMT8(-/-) knockout mice presented with altered membrane phospholipid composition, decreased mitochondrial stress capacity, and increased neuroinflammatory markers, such as tumor necrosis factor alpha and ionized calcium binding adaptor molecule 1 (Iba1, a specific marker for microglia/macrophage activation) after hypoxic stress. Furthermore, adenovirus-based overexpression of PRMT8 reversed the changes in membrane phospholipid composition, mitochondrial stress capacity, and neuroinflammatory markers. Together, our findings establish PRMT8 as an important regulatory component of membrane phospholipid composition, short-term memory function, mitochondrial function, and neuroinflammation in response to hypoxic stress.

摘要

精氨酸甲基转移酶（PRMTs）是一类参与基因调控和蛋白质/组蛋白修饰的酶。PRMT8 主要在中枢神经系统中表达，特别是在细胞膜和突触小泡中。最近，PRMT8 被描述为在神经元信号转导中发挥关键作用，例如树突分支、突触功能和成熟、神经元分化和可塑性的调节剂。在这里，我们研究了 PRMT8 在应对脑代谢缺氧应激中的作用。我们的液相色谱质谱、线粒体耗氧率和蛋白质分析结果表明，PRMT8(-/-) 敲除小鼠在缺氧应激后表现出膜磷脂组成改变、线粒体应激能力下降和神经炎症标志物增加，如肿瘤坏死因子-α和离子钙结合衔接蛋白 1（Iba1，小胶质细胞/巨噬细胞激活的特异性标志物）。此外，腺病毒过表达 PRMT8 逆转了膜磷脂组成、线粒体应激能力和神经炎症标志物的变化。总之，我们的研究结果确立了 PRMT8 作为应对缺氧应激时膜磷脂组成、短期记忆功能、线粒体功能和神经炎症的重要调节成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/627f/8595568/802b58ca5708/nihms-1721802-f0011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/627f/8595568/a9ed22d77f4c/nihms-1721802-f0006.jpg
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