期刊
BRAIN INJURY
卷 35, 期 11, 页码 1462-1471出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/02699052.2021.1972156
关键词
Cerebral ischemia reperfusion injury; linc00473; ceRNA; srpk1
Our study revealed the protective role of LINC00473 in cerebral I/R injury, suggesting it may serve as a novel target for treating ischemic brain injury.
Background Cerebral ischemia is associated with a high burden of neurological disability. Recently, emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) are crucial regulators in cerebral ischemia reperfusion (I/R) injury. Herein, we investigated the function and potential mechanism of long intergenic non-protein coding RNA 473 (LINC00473) in cerebral I/R injury. Methods We established oxygen glucose deprivation/reperfusion (OGD/R) model in Neuro-2a (N2a) cells to mimic the cerebral I/R injury in vitro. RT-qPCR and Western blot assays were conducted to detect target gene expression. Functional assays measured the effects of LINC00473 on cell viability, apoptosis and reactive oxygen species (ROS) production. A series of mechanism assays were carried out to detect the potential mechanism of LINC00473 in cerebral I/R injury. Results LINC00473 was significantly down-regulated in OGD/R-induced injury model. LINC00473 overexpression reversed the reduced cell viability as well as the enhanced apoptosis and ROS level induced by OGD/R. Moreover, LINC00473 functioned as a competing endogenous RNA (ceRNA) to sponge miR-15b-5p and miR-15a-5p and thereby regulated SRSF protein kinase 1 (SRPK1) expression. Conclusions Our findings confirmed the protective role of LINC00473 in cerebral I/R injury, which might provide a novel target for treating ischemic brain injury.
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