Microglia regulates the proliferation of OPCs after spinal cord injury through STAT3
Objective This study aims to investigate the regulatory role of microglia(Mg)on oligodendrocyte progenitor cells(OPCs)following spinal cord injury(SCI)and explore potential molecular mechanisms.The goal is to provide a theoretical and experimental basis for the clinical treatment of SCI.Methods An in vitro co-culture system of Mg and OPCs was established.Mg were activated using lipopolysaccharide(LPS).The impact of Mg on OPC proliferation and the expression of signal transducer and activator of transcription 3(STAT3),closely associated with proliferation,were examined using immunofluorescence and Western blot methods.A mouse SCI model was created,and changes in STAT3 expression were monitored at different time points post-injury(1,3,7,14 days).The CSF1R inhibitor PLX3397 was employed to eliminate mouse microglia,and its effect on OPC proliferation and STAT3 expression was investigated.Results Following LPS stimulation,Mg cell bodies significantly enlarged(P＜0.05),and the cell population increased significantly(P＜0.05).Activated Mg promoted OPC proliferation through STAT3 activation(P＜0.05),a function inhibited by the STAT3 inhibitor STA21(P＜0.05).After SCI,STAT3 expression in the spinal cord significantly increased(P＜0.05),peaking on the 3rd day post-injury.The elimination of Mg reduced STAT3 expression in the spinal cord and inhibited oligodendrocyte proliferation.Conclusion Mg may promote OPC proliferation after SCI through the activation of STAT3.
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