scholarly journals Exosomes secreted by stem cells from human exfoliated deciduous teeth contribute to functional recovery after traumatic brain injury by shifting microglia M1/M2 polarization in rats

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Ye Li ◽  
Yuan-Yuan Yang ◽  
Jia-Li Ren ◽  
Feng Xu ◽  
Fa-Ming Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Brain Injury ◽  
Functional Recovery ◽  
Deciduous Teeth ◽  
M2 Polarization ◽  
Human Exfoliated Deciduous Teeth

scholarly journals SHED-Derived Exosomes Regulate Microglial Polarization in the Treatment of Traumatic Brain Injury in Rats via miR-330-5p

2020 ◽  
Author(s):  
Ye Li ◽  
Xinxin Wang ◽  
Xiaoyu Cao ◽  
Na Li ◽  
Sun Meng ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Structural Damage ◽  
Inhibitory Effect ◽  
Deciduous Teeth ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Polarization ◽  
M1 Polarization

Abstract Background: Traumatic brain injury (TBI) causes structural damage and impairs motor and cognitive function of the brain. Our previous study suggested that exosomes (EXs) secreted by stem cells from human exfoliated deciduous teeth (SHED) extenuated motor damage in TBI rats by regulating microglia. The molecular mechanism of SHED-EXs was investigated in the present study. Methods: The miRNA array was performed to determine the differential miRNA expression in SHED-EXs treating microglia. The key miRNA was selected. Flow cytometry, immunofluorescence, enzyme linked immunosorbent assay (ELISA) and Griess assay were performed to detect the function of key miRNA. Real-time PCR, Western blotting and dual luciferase reporter assay were used to confirm the relationship between key miRNA and the target gene. Chromatin immunoprecipitation (ChIP) was performed to determine the downstream pathway of EXs-miRNA. Traumatic brain injury rat model was established and local injection of EXs-miRNA was performed to evaluate the effect.Results: SHED-EXs delivery of miR-330-5p was the key in the regulation of microglia polarization by inhibiting M1 polarization and promoting M2 polarization. Mechanistically, miR-330-5p had an inhibitory effect on Ehmt2, and miR-330-5p/Ehmt2 promoted the transcription of CXCL14 through H3K9me2. In vivo data showed that SHED-EXs/miR-330-5p reduced neuro-inflammation and repaired neurological function of TBI rats. Conclusions: SHED-EXs/miR-330-5p improved the motor function of rats after TBI by inhibiting M1 polarization and promoting M2 polarization of microglia through Ehmt2/H3K9me2/CXCL14 pathway.

scholarly journals Ectoderm-Derived Frontal Bone Mesenchymal Stem Cells Promote Traumatic Brain Injury Recovery by Alleviating Neuroinflammation and Glutamate Excitotoxicity

2021 ◽  
Author(s):  
Qiaozhen Qin ◽  
Ting Wang ◽  
Zhenhua Xu ◽  
Shuirong Liu ◽  
Heyang Zhang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Brain Injury ◽  
Functional Recovery ◽  
Frontal Bone ◽  
Neural Regeneration ◽  
Glutamate Excitotoxicity ◽  
Bone Mesenchymal Stem Cells ◽  
Injury Recovery

Abstract Traumatic brain injury (TBI) leads to cell and tissue impairment, as well as functional deficits. Stem cells promote structural and functional recovery and thus are considered as a promising therapy for various nerve injuries. Here, we aimed to investigate the role of ectoderm-derived frontal bone mesenchymal stem cells (FbMSCs) in promoting cerebral repair and functional recovery in a murine TBI model. FbMSCs showed fibroblast like morphology and osteogenic differentiation capacity. FbMSCs were CD105, CD29 positive and CD45, CD31 negative. Different from mesoderm-derived MSCs, FbMSCs highly expressed ectoderm-specific transcription factor Tfap2β and growth factor FGF1. FbMSC application significantly ameliorated the behavioral deficits of TBI mice and promoted neural regeneration. Immunofluorescence staining and qRT-PCR data revealed that microglial activation and astrocyte polarization to the A1 phenotype were suppressed by FbMSC application. In addition, FGF1 secreted from FbMSCs enhanced glutamate transportation by astrocytes and alleviated the cytotoxic effect of excessive glutamate on neurons. Therefore, MSCs with characteristics of FbMSCs might be good candidates for TBI therapy.

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