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Journal Article

Citation

Xu C, Fu F, Li X, Zhang S. Int. J. Neurosci. 2017; 127(12): 1124-1135.

Affiliation

Institution of brain trauma and neurology disease of affiliated hospital of Logistics university of PAP , Tianjin , China.

Copyright

(Copyright © 2017, Informa - Taylor and Francis Group)

DOI

10.1080/00207454.2017.1325884

PMID

28464695

Abstract

Mesenchymal Stem Cells (MSCs), which are regarded as promising candidates for cell replacement therapies, are able to regulate immune responses after traumatic brain injury (TBI). Secondary immune response following the mechanical injury is the essential factor leading to the necrosis and apoptosis of neural cells during and after the cerebral edema has subsided and there is lack of efficient agent that can mitigate such neuroinflammation in the clinical application. By means of three molecular pathways (prostaglandin E2 (PGE2), tumor necrosis factor-inducible gene 6 protein (TSG-6), and progesterone receptor (PR) and glucocorticoid receptors (GR)), MSCs induce the activation of macrophages/microglia and drive them polarize into the M2 phenotypes, which inhibits the release of pro-inflammatory cytokines and promotes tissue repair and nerve regeneration. The regulation of MSCs and the polarization of macrophages/microglia are dynamically changing which based on the inflammatory environment. Under the stimulation of platelet lysate (PL), MSCs also promote the release of pro-inflammatory cytokines. Meanwhile, the statue of macrophages/microglia exerts significant effects on the survival, proliferation, differentiation and activation of MSCs by changing the niche of cells. They form positive feedback loops in maintaining the homeostasis after TBI to relieving the secondary injury and promoting tissue repair. MSCs therapies have obtained great achievements in several CNS diseases clinical trials, which will accelerate the application of MSCs in TBI treatment.


Language: en

Keywords

cell based therapy; macrophage/microglia polarization; mesenchymal stem cells; neuroinflammation; traumatic brain injury

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