Carbon monoxide preconditioning is mediated via activation of mitochondrial-derived vesicles

被引:6
|
作者
Guo, Ying [1 ,2 ]
Guan, Teng [1 ]
Jiao, Xin [2 ]
Tian, Xiaofei [2 ]
Jin, Chunting [2 ]
Zhang, Guohui [2 ]
Kong, Jiming [1 ,2 ]
机构
[1] Univ Manitoba, Dept Human Anat & Cell Sci, 745 Bannatyne Ave, Winnipeg, MB R3E 0J9, Canada
[2] Hebei North Univ, Dept Forens Med, 11 South Diamond Rd, Zhangjiakou 075000, Hebei, Peoples R China
关键词
Carbon monoxide; Preconditioning; Oligodendrocytes; Mitochondria -derived vesicles; Mitochondrial quality control; PROTECTION; TRANSPORT; PINK1; CARGO;
D O I
10.1016/j.brainresbull.2023.02.011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Preconditioning with inhalative carbon monoxide (CO) at low concentrations provides protection against hyp-oxic and ischemic insults in the brain and heart. The present study aims to test a hypothesis that activation of mitochondrial-derived vesicles (MDVs) is a mechanism underlying the protective effect of CO preconditioning. Here we show that CO preconditioning induced mild oxidative stress and activated massive production of MDVs. Short exposure to a low concentration of carbon monoxide-releasing molecule 2 (CORM-2), a donor of carbon monoxide, prevented oligodendrocyte precursor cells (OPCs) from subsequent death induced by high doses of CO, and protected Chinese hamster ovary (CHO) cells against oxygen-glucose deprivation (OGD)-induced cell death. Furthermore, inhibition of lysosomal activity prevented degradation of MDVs, abolished MDV-mediated mitochondrial quality control, and diminished the protective effect of CO preconditioning. Altogether, our data provide direct evidence suggesting that MDV-mediated mitochondrial quality control may have a novel role in CO preconditioning.
引用
收藏
页码:99 / 108
页数:10
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