1. LINC00473 protects against cerebral ischemia reperfusion injury via sponging miR-15b-5p and miR-15a-5p to regulate SRPK1 expression.
- Author
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Yao, Boxin, Ye, Lichao, Chen, Jixing, Zhuo, Shitu, and Lin, Huasong
- Subjects
GLUCOSE metabolism ,OXYGEN metabolism ,RNA physiology ,BIOMARKERS ,BIOLOGICAL models ,REVERSE transcriptase polymerase chain reaction ,IN vitro studies ,ANIMAL experimentation ,WESTERN immunoblotting ,APOPTOSIS ,GENE expression ,CELL survival ,CELL lines ,REACTIVE oxygen species ,POLYMERASE chain reaction ,CEREBRAL ischemia ,REPERFUSION injury ,MICE - Abstract
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. 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. 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 functioneds as a competing endogenous RNA (ceRNA) to sponge miR-15b-5p and miR-15a-5p and thereby regulated SRSF protein kinase 1 (SRPK1) expression. Our findings confirmed the protective role of LINC00473 in cerebral I/R injury, which might provide a novel target for treating ischemic brain injury. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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