Neuroinflammation in Ischemic Stroke: Focus on MicroRNA-mediated Polarization of Microglia.

Lu Lian,Shixin Xu,Lu Liu,Liji Yang,Yichen Cai,Junping Zhang,Yunsha Zhang

doi:10.3389/fnmol.2020.612439

Abstract

Ischemic stroke is one of the most common causes of death and disability worldwide. Neuroinflammation is a major pathological event involved in the process of ischemic injury and repair. In particular, microglia play a dual role in neuroinflammation. During the acute phase of stroke onset, M2 microglia are the dominant phenotype and exert protective effects on neuronal cells, whereas permanent M1 microglia contribute to prolonged inflammation and are detrimental to brain tissue. Emerging evidence indicates that microRNAs (miRNAs) may have regulatory effects on microglia-associated inflammation. Thus, we briefly reviewed the dynamic response of microglia after a stroke and assessed how specific miRNAs affect the behavior of reactive microglia. We concluded that miRNAs may be useful novel therapeutic targets to improve stroke outcomes and modulate neuroinflammation.

Highlights

Ischemic stroke is one of the most common causes of death and disability worldwide (Chen et al, 2019)
Similar to the data on the surface markers CD68, Ym1, and CD206, other studies have shown that the expression of M2 phenotype related genes, including Arg1, CCL22, Ym1/2, IL-10, and TNF-α, increased progressively within 24 h after MCAO and reached a peak after 3–5 d (Hu et al, 2012) (In contradiction with the previously presented data, this study indicated that the M2 related-gene have a different expression pattern than previously described)
Most studies on microglial phenotypes have focused on the process through which miRNAs reduce pro-inflammatory responses, while less attention has been paid to the antiinflammatory effects shown by the M2 phenotype

Summary

Introduction

Ischemic stroke is one of the most common causes of death and disability worldwide (Chen et al, 2019). MiR-203 regulates the NF-κB signaling via negative feedback by directly targeting the myeloid differentiation primary response gene 88, which leads to the activation of microglia, and promotes the release of inflammatory factors.

Results

Conclusion