These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Bone marrow mesenchymal stem cell-derived exosomal microRNA-125a promotes M2 macrophage polarization in spinal cord injury by downregulating IRF5.
    Author: Chang Q, Hao Y, Wang Y, Zhou Y, Zhuo H, Zhao G.
    Journal: Brain Res Bull; 2021 May; 170():199-210. PubMed ID: 33609602.
    Abstract:
    BACKGROUND: Spinal cord injury (SCI) may cause loss of locomotor function, and macrophage is a major cell type in response to SCI with M1- and M2-phenotypes. The protective role of bone marrow mesenchymal stem cells (BMMSC)-derived exosomes (B-Exo) in SCI has been underscored, while their regulation on M2 macrophage polarization and the mechanism remain to be clarified. METHODS: A rat model of SCI was developed and treated with extracted B-Exo. Recovery of motor function was assessed by Basso-Beattie-Bresnahan (BBB) score. The apoptosis and degeneration of neurons, and macrophage polarization were evaluated. Subsequently, genes differentially expressed in the rat spinal cord after B-Exo treatment were analyzed. Later, the relationships between B-Exo and interferon regulatory factor 5 (IRF5) or macrophage polarization were clarified. Later, the upstream microRNAs (miRNAs) of IRF5 were validated by bioinformatics prediction and dual-luciferase experiments. Finally, the role of miR-125a in the neuroprotection of SCI was verified by rescue experiments. RESULTS: B-Exo promoted the recovery of locomotor function and M2-phenotype polarization, whereas inhibited neuronal apoptosis and degeneration and the inflammatory response caused by SCI in rats. In addition, IRF5 expression was reduced after B-Exo treatment. IRF5 promoted macrophage polarization towards M1-phenotype and secretion of inflammatory factors. There is a binding relationship between miR-125a and IRF5. Knockdown of miR-125a in B-Exo increased IRF5 expression in spinal cord tissues of SCI rats and attenuated the neuroprotective effect of B-Exo against SCI. CONCLUSION: Exosomal miR-125a derived from BMMSC exerts neuroprotective effects by targeting and negatively regulating IRF5 expression in SCI rats.
    [Abstract] [Full Text] [Related] [New Search]