Dual roles of microglia in the pathological injury and repair of hemorrhagic cerebrovascular diseases

Tan, Lulin1; Liang, Jingyan1,2; Wang, Xingyi1; Wang, Yingge1,2,3; Xiong, Tianqing1,2,3,4

1Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu Province, China

2Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research, Yangzhou University, Yangzhou, Jiangsu Province, China

3Department of Neurology, Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu Province, China

4Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA

*Correspondence to: Tianqing Xiong, 007418@yzu.edu.cn.

Funding: This work was supported by the China Postdoctoral Science Foundation, No. 2022M712689, the Natural Science Foundation of the Jiangsu Higher Education Institutions of China, No. 22KJB1800029, the China International Medical Foundation of Cerebrovascular Disease Youth Innovation Fund, No. Z-2016-20-2101, and the Medical Innovation and Translation Special Fund of Yangzhou University “Clinical Translation Research Project,” No. AHZZUZHXM 202102.

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Regenerative Medicine Reports 1(1):p 93-105, September 2024. | DOI: 10.4103/RMR.REGENMED-D-24-00001

Abstract

Microglia are one of the most important immune cells in the central nervous system, which mainly play an immune surveillance role under normal conditions to maintain central nervous system homeostasis. In the early stages of hemorrhagic brain injury, microglia are activated to the classical phenotype (M1 type). At this time, microglia can promote the inflammatory response by secreting inflammatory cytokines and reactive oxygen species, thereby disrupting the blood–brain barrier. Consequently, this leads to neuronal cell necrosis, aggravates brain edema, and triggers secondary brain injury. However, in the later stages of hemorrhagic brain injury, microglia can switch from the M1 phenotype to the alternative activating M2 phenotype. This transition allows them to participate in the repair process of the nervous system after a brain hemorrhage. They achieve this by phagocytosing tissue debris, secreting anti-inflammatory cytokines, and releasing growth factors to suppress the overacting inflammatory response and promote angiogenesis. Therefore, this paper presents an account of cerebral hemorrhage and subarachnoid hemorrhage, with a primary focus on exploring the role of microglia in hemorrhagic cerebrovascular disease. The aim is to provide new perspectives for basic and clinical translational research in hemorrhagic cerebrovascular disease.

小胶质细胞在出血性脑血管病损伤和修复中的双重作用

摘要

小胶质细胞是中枢神经系统中最重要的免疫细胞之一，在正常条件下主要发挥免疫监视作用，可维持中枢神经系统稳态。在出血性脑损伤的早期阶段，小胶质细胞激活成为经典表型（M1型）。此时，小胶质细胞可通过分泌炎性细胞因子和活性氧来促进炎症反应，从而破坏血脑屏障，进而导致神经元细胞坏死，加重脑水肿，并引发继发性脑损伤。然而，在出血性脑损伤的后期，小胶质细胞则可从M1表型转换为替代激活M2表型。这种转变使其能够参与脑出血后神经系统的修复过程。M2型小胶质细胞可通过吞噬组织碎片、分泌抗炎细胞因子和释放生长因子来抑制过度炎症反应并促进血管生成。此次综述对脑出血和蛛网膜下腔出血中小胶质细胞作用进行总结，这将为出血性脑血管病的基础研究和临床转化研究提供帮助。