title: Effect of Extracellular Vesicles on Neural Functional Recovery and Immunologic Suppression after Rat Cerebral Apoplexy.
abstract: BACKGROUND
  Previous studies have demonstrated that mesenchymal stem cells (MSCs) can promote the recovery of neural function after cerebral apoplexy by secreting multiple cytokines. In addition, cell factor-derived extracellular vesicles play an important role in recovery of neural function. The aim of this study was to determine the effect of extracellular vesicles on neural functional recovery and brain tissue remodeling after cerebral apoplexy in a rat model.
  
  
  METHODS
  The rat models with local ischemic stroke was established and three random groups were created. In groups A and B, human bone marrow-derived MSCs and MSC-derived extracellular vesicles were transplanted into rats. In the control group (group C), only normal saline was injected. Then, we evaluated motor coordination ability, pathologic changes of the brain, immune responses in the central and peripheral nervous systems, regeneration of blood vessels, and nervous tissue in 4 weeks after cerebral apoplexy.
  
  
  RESULTS
  Obvious regeneration of blood vessels and nervous tissues were identified in groups A and B. There was no significant difference with respect to coordination between groups A and B, but coordination in groups A and B was significantly better than the control group. Immunohistochemical staining of brain tissue showed that extracellular vesicles exerted no effect on infiltration of immune cells in the central nervous system. Weakened immune suppression was noted 1 week after cerebral apoplexy, which provided a favorable environment for remodeling of brain tissue.
  
  
  CONCLUSIONS
  MSC-derived extracellular vesicles accelerated neural functional recovery after cerebral apoplexy. The weakened immune suppression was beneficial to remodeling of brain tissue.
authors.affiliation: Department of Neurology, The 2nd Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
authors.forename: Beilei
authors.initials: B
authors.lastname: Hu
authors.forename: Songfang
authors.initials: S
authors.lastname: Chen
authors.forename: Ming
authors.initials: M
authors.lastname: Zou
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: He
authors.forename: Shengmin
authors.initials: S
authors.lastname: Shao
authors.forename: Baohua
authors.initials: B
authors.lastname: Liu
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D002452:Cell Count; D000067128:Extracellular Vesicles / Q000378:metabolism*; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D037181:Lectins, C-Type / Q000378:metabolism; D017493:Leukocyte Common Antigens / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000166:cytology; D051379:Mice; D009069:Movement Disorders / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D009474:Neurons / Q000473:pathology*; D051381:Rats; D020127:Recovery of Function; D020521:Stroke / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000949:Histocompatibility Antigens Class II; D037181:Lectins, C-Type; D017493:Leukocyte Common Antigens; D000099192:CD69 Antigens