Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1.

Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1. Exp Neurol. 2019 Jan 28;: Authors: Wei R, Zhang L, Hu W, Wu J, Zhang W Abstract Emerging evidence has suggested a significant role of long non-coding RNAs (lncRNAs) in ischemic stroke by acting as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs) to regulate certain RNA transcripts. AK038897 is an lncRNA that was reported to be upregulated in rat brains in response to transient focal ischemia. We aimed to investigate the possible regulatory role of AK038897 in ischemic stroke. We detected increased AK038897 and decreased miR-26a-5p levels in mouse brains following middle cerebral artery occlusion/reperfusion (MCAO/R) and in neuro-2A (N2a) neuroblastoma cells following oxygen-glucose deprivation and reoxygenation (OGD/R). With bioinformatics, we identified shared putative miR-26a-5p binding sites in AK038897 as well as in the 3'-UTR of death-associated protein kinase 1 (DAPK1), which is a central mediator of ischemic neuronal death. MiR-26a-5p overexpression attenuated OGD/R-induced N2a cell apoptosis. The luciferase reporter assay results confirmed that miR-26a-5p directly targets DAPK1. Further studies showed that AK038897 directly binds to miR-26a-5p and functions as a ceRNA for miR-26a-5p to regulate DAPK1. As a result, AK038897 overexpression antagonized while AK038897 knockdown enhanced the i...
Source: Experimental Neurology - Category: Neurology Authors: Tags: Exp Neurol Source Type: research