HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation.
HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation.
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DOI：
10.1155/2022/9030771
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发表时间：
2022
影响因子：
--
通讯作者：
He X
中科院分区：
文献类型：
--
作者：
Ye Y;Feng Z;Tian S;Yang Y;Jia Y;Wang G;Wang J;Bai W;Li J;He X
由于脑卒中患者的神经发生能力有限，长期以来，如何更好地从脑卒中引起的神经功能障碍中恢复一直是一个很大的挑战。神经干细胞程序性死亡是脑卒中后神经再生的不利因素之一。神经干细胞的凋亡和坏死性凋亡等死亡类型已得到深入研究，而神经干细胞的焦亡还不十分清楚。高压氧（HBO）可减轻脑卒中后神经干细胞的缺糖缺氧（OGD）损伤，减少其程序性死亡，但其是否参与了脑卒中后神经干细胞的凋亡尚不清楚。因此，本研究的目的是研究高压氧处理对OGD暴露后NSC焦亡的潜在影响，以及其对体外NSC增殖和分化的影响。结果表明，OGD增加NOD样受体蛋白3（NLRP 3）的表达，诱导神经干细胞的热凋亡，这是由高压氧治疗挽救。上调的lncRNA-H19作为miR-423- 5 p的分子海绵，靶向NLRP 3，参与OGD后NSC的热凋亡。最重要的是，证实了HBO通过抑制lncRNA-H19/miR-423- 5 p/NLRP 3轴来保护NSC免受焦亡。此外，HBO抑制lncRNA-H19相关的细胞凋亡有利于神经干细胞的增殖和神经元分化。结论HBO通过lncRNA-H19/miR-423- 5 p/NLRP 3轴减轻NSC的焦亡，并增强OGD后的神经发生。这些发现为脑卒中后NSC程序性死亡提供了新的认识，并启发了治疗策略。
Due to the limited neurogenesis capacity, there has been a big challenge in better recovery from neurological dysfunction caused by stroke for a long time. Neural stem cell (NSC) programmed death is one of the unfavorable factors for neural regeneration after stroke. The types of death such as apoptosis and necroptosis have been deeply investigated while the pyroptosis of NSCs is not quite understood. Although it is well accepted that hyperbaric oxygen (HBO) alleviates the oxygen-glucose deprivation (OGD) injury after stroke and reduces programmed death of NSCs, whether NSC pyroptosis is involved in this process is still unknown. Therefore, this study is aimed at studying the potential effect of HBO treatment on NSC pyroptosis following OGD exposure, as well as its influence on NSC proliferation and differentiation in vitro. The results revealed that OGD increased NOD-like receptor protein 3 (NLRP3) expression to induce the pyroptotic death of NSCs, which was rescued by HBO treatment. And the upregulated lncRNA-H19 functioned as a molecular sponge of miR-423-5p to target NLRP3 for NSC pyroptosis following OGD. Most importantly, it was confirmed that HBO exerted protection of NSCs against pyroptosis by inhibiting lncRNA-H19/miR-423-5p/NLRP3 axis. Moreover, HBO restraint of lncRNA-H19-associated pyroptosis benefited the proliferation and neuronal differentiation of NSCs. It was concluded that HBO attenuated NSC pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 axis and enhanced neurogenesis following OGD. The findings provide new insight into NSC programmed death and enlighten therapeutic strategy after stroke.
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