M1 Microglia Induced Neuronal Injury on Ischemic Stroke via Mitochondrial Crosstalk between Microglia and Neurons

Author:

Liu Wei1ORCID,Qi Zitong1ORCID,Li Wanmeng1ORCID,Liang Jia2ORCID,Zhao Liang1ORCID,Shi Yijie1ORCID

Affiliation:

1. School of Pharmacy, Jinzhou Medical University, Jinzhou 121000, China

2. Life Science Institution, Jinzhou Medical University, Jinzhou 121000, China

Abstract

Among the middle-aged and senile populations, ischemic stroke (IS) is a frequently occurring acute condition of the cerebrovascular system. Traditionally, it is recognized that when stroke occurs, microglia are activated into M1 phenotype and release cytotoxic cytokines, reactive oxygen species, proteases, and other factors, thus exacerbating the injury by further destroying or killing nearby neurons. In the latest research, the crucial role of the intercellular mitochondrial crosstalk on the stroke management has been demonstrated. Therefore, we tried to clarify mitochondrial crosstalk between microglia and neurons, and evaluated M1 microglial mitochondria-mediated neurological performance in transient middle cerebral artery occlusion (tMCAO) rats. We found that when microglia was activated into the proinflammatory M1 type after stroke, mitochondrial fission process was accelerated, and damaged mitochondria were released, further transferred to neurons and fused with neuronal mitochondria. As a result, the function of neuronal mitochondria was damaged by decreasing adenosine triphosphate (ATP), mitochondria membrane potential, and increasing excessive reactive oxygen species (ROS), thus inducing mitochondria-mediated neuronal death and finally aggravating ischemia injury. Taken together, it provides a novel neuroglial crosstalk mechanism at the mitochondrial level.

Funder

2021 Youth Science and Technology Talents Support Plan from Boze Project of Jinzhou Medical University

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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