scholarly journals A Novel Cerebroprotein Hydrolysate, CH1, Ameliorates Chronic Focal Cerebral Ischemia Injury by Promoting White Matter Integrity via the Shh/Ptch-1/Gli-1 Signaling Pathway

2020 ◽  
Vol Volume 16 ◽  
pp. 3209-3224
Author(s):  
Wen Cao ◽  
Cong Zhang ◽  
Rong Chen ◽  
Qianqian Wu ◽  
Renhao Xu ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Signaling Pathway ◽  
Focal Cerebral Ischemia ◽  
White Matter Integrity ◽  
Gli 1

scholarly journals Rosiglitazone Promotes White Matter Integrity and Long-Term Functional Recovery After Focal Cerebral Ischemia

Stroke ◽  
2015 ◽  
Vol 46 (9) ◽  
pp. 2628-2636 ◽  
Author(s):  
Lijuan Han ◽  
Wei Cai ◽  
Leilei Mao ◽  
Jia Liu ◽  
Peiying Li ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Functional Recovery ◽  
Focal Cerebral Ischemia ◽  
White Matter Integrity

Abstract TMP30: M2 Microglia Derived Exosomes Promote White Matter Repair and Long-Term Functional Recovery After Focal Cerebral Ischemia in Mice

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yongfang Li ◽  
Longlong Luo ◽  
Zhijun Zhang ◽  
Yaohui Tang ◽  
Guo-Yuan Yang
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor Cell ◽  
M2 Microglia ◽  
Oligodendrocyte Precursor ◽  
White Matter Repair ◽  
Exosomal Mirna

Objectives: White matter injury aggravates neurological and cognitive impairment in experimental ischemic stroke. M2 microglia promote oligodendrocyte precursor cells survival and differentiation, and further enhance white matter repair. However, the molecular mechanism is unclear. Here, we explored the effect and mechanism of M2 microglia-derived exosomes on white matter repair after focal cerebral ischemia in mice. Methods: Microglia BV2 cells were polarized to M2 phenotype by IL-4 stimulation. Exosomes were isolated from M2 microglia (M2-Exo) and unstimulated microglia as a control (M0-Exo). M2-Exo and M0-Exo (100 μg) were intravenously injected after 90-minute middle cerebral artery occlusion in mice (n=72). Brain atrophy volume and neuro behavioral outcomes were examined in 28 days following focal cerebral ischemia. Oligodendrocyte precursor cells survival, differentiation and white matter integrity were evaluated. Exosomal miRNA and target gene were further examined to explore molecular mechanism. Results: M2-Exo treatment promoted sensorimotor and memory function recovery ( p <0.05), and further reduced brain atrophy compared to the M0-Exo control group ( p <0.001). Immunostaining showed that M2-Exo increased the number of BrdU + /Pdgfr-α + and BrdU + /adenomatous polyposis coli + cells, enhanced myelin basic protein fluorescence-intensity compared to the control ( p <0.05). M2-Exo increased oligodendrocyte precursor cell survival under OGD in vi tro , ( p <0.05) and differentiation ( p <0.05). Exosomal miRNA sequencing and PCR identified that miR-23a-5p was enriched in M2-Exo. Conclusion: Our results showed that M2-Exo treatment enhanced oligodendrocyte precursor cell survival and differentiation, further promoted white matter repair and long-term functional recovery, suggesting that M2-Exo is a novel therapeutic strategy for the white matter repair after ischemic brain injury.

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