LINC00473 protects against cerebral ischemia reperfusion injury via sponging miR-15b-5p and miR-15a-5p to regulate SRPK1 expression

• Published in: Brain injury 2021-09, Vol.35 (11), p.1462-1471
• Main Authors: Yao, Boxin, Ye, Lichao, Chen, Jixing, Zhuo, Shitu, Lin, Huasong
• Format: Article
• Language: English
• Subjects: Apoptosis - genetics; Brain Ischemia - genetics; Cerebral ischemia reperfusion injury; ceRNA; Humans; linc00473; MicroRNAs - genetics; Protein Serine-Threonine Kinases; Reperfusion Injury - genetics; RNA, Long Noncoding - genetics; srpk1
• ISSN: 0269-9052; 1362-301X
• DOI: 10.1080/02699052.2021.1972156

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.