MSCs-Derived Exosomes Attenuate Acute Brain Injury and Inhibit Microglial Inflammation by Reversing CysLT2R-ERK1/2 Mediated Microglia M1 Polarization

Neurochem Res. 2020 May;45(5):1180-1190. doi: 10.1007/s11064-020-02998-0. Epub 2020 Feb 28.

Abstract

Inflammatory responses play a major role in the pathophysiology of cerebral ischemia. Mesenchymal stem cell-derived exosomes (MSC-exos) have important anti-inflammatory effects on the treatment of organ injury. This study aimed to determine the anti-inflammatory effect and furtherly investigate the potential mechanism of MSC-exos on acute cerebral ischemia. MSC-exos were isolated by ultracentrifugation, characterized by transmission electron microscopy and FACS. Rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) surgery were administered MSC-exos through the tail vein. In vitro, microglia exposed to oxygen- and glucose-deprivation (OGD) and leukotrienes were used to study the protective mechanism of exosomes against ischemia/reperfusion-induced inflammation. The intake of exosomes into microglia was visualized through immunofluorescence staining. The results showed that MSC-exos treatment significantly improved motor, learning and memory abilities of MCAO/R rats 7 days later. The production of pro-inflammatory factors decreased, while the anti-inflammatory cytokines and neurotrophic factors increased both in the cortex and hippocampus of ischemic hemisphere as well as in the culture supernatant of microglia treated with OGD and NMLTC4. MSC-exos treatment also significantly inhibited M1 microglia polarization and increased M2 microglia cells. Furthermore, western blot analysis demonstrated that CysLT2R expression and ERK1/2 phosphorylation were downregulated both in vivo and in vitro. Thus, MSC-exos attenuated brain injury and inhibited microglial inflammation by reversing CysLT2R-ERK1/2 mediated microglia M1 polarization.

Keywords: CysLT2R; Exosome; Inflammation; M1 microglia polarization; MSCs.

MeSH terms

  • Animals
  • Brain Injuries / metabolism*
  • Brain Injuries / therapy
  • Cell Polarity
  • Cells, Cultured
  • Exosomes / transplantation*
  • Inflammation / metabolism
  • Inflammation / therapy
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism
  • MAP Kinase Signaling System / physiology*
  • Male
  • Mesenchymal Stem Cell Transplantation / methods*
  • Mesenchymal Stem Cells
  • Microglia / metabolism*
  • Microglia / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Leukotriene / metabolism*

Substances

  • Inflammation Mediators
  • Receptors, Leukotriene
  • cysteinyl leukotriene receptor 2