| First Author | Cao Y | Year | 2021 |
| Journal | Neuroscience | Volume | 458 |
| Pages | 64-76 | PubMed ID | 33075457 |
| Mgi Jnum | J:305346 | Mgi Id | MGI:6709991 |
| Doi | 10.1016/j.neuroscience.2020.10.010 | Citation | Cao Y, et al. (2021) Long Non-coding RNA TALNEC2 Aggravates Cerebral Ischemia/Reperfusion Injury via Acting as a Competing Endogenous RNAs for miR-650 to Target Apoptotic Peptidase Activating Factor 1. Neuroscience 458:64-76 |
| abstractText | Increasing evidence has indicated that long non-coding RNAs (lncRNAs) play a vital role for adjusting RNA transcripts as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs). The present study was intended to explore the probable regulation of lncRNA TALNEC2 in ischemic stroke. In this study, we measured the up-regulation of TALNEC2 and down-regulation of miR-650 in mice brains after cerebral ischemia/reperfusion (I/R) operation and in cultured neuroblastoma cells of neuro-2A (N2a) treated with oxygen glucose deprivation/reoxygenation (OGD/R). Then we verified the common predicted binding sites of miR-650 in TALNEC2 and 3'-UTR of apoptotic peptidase activating factor 1 (APAF1), a critical regulator in ischemic neuronal death, with bioinformatics. Overexpression of miR-650 reduced N2a cell apoptosis induced by OGD/R. MiR-650 was confirmed to be a directly target of APAF1 by luciferase reporter assay. It was found that TALNEC2 played a critical role as a ceRNA for miR-650 and bound directly to miR-650 to mediate the APAF1. In result, overexpression of TALNEC2 antagonized the inhibition impact of miR-650 on APAF1 expression and N2a cell apoptosis induced by OGD/R, while TALNEC2 knockdown aggravated the impact. Furthermore, TALNEC2 knockdown reversed brain injury and neurological deficits induced by I/R in vivo. In conclusion, we verified a TALNEC2/miR-650/APAF1 signaling pathway as a key mechanism monitoring cerebral I/R injury. |
