Liu Yang1, Yin Xiong1, Xian-Feng Hu1, Yan-Hua Du1. 1. Department of Geratology, Pu Ai Hospital of Tongji Medical College, Huazhong University of Science and Technology Wuhan 430033, China.
Abstract
PURPOSE: MicroRNA-323 (miR-323) has been reported to be upregulated in Ischemia/Reperfusion (I/R) injury-treated neuronal cell. However, the effect and underlying mechanism of miR-323 in I/R-induced neuronal cell death remains poorly understood. The current study was aim to investigate the role and molecular basis of miR-323 in I/R-induced neuronal cell. METHODS: An oxygen-glucose deprivation (OGD) model of hippocampal neuron I/R was produced in vitro. Cell apoptosis, cell survival, and the expression of miR-323 were determined after 6 h, 12 h and 24 h after OGD treatment. The up- or down-regulation of miR-323 was performed by miR-323 mimics or anti-miR-323, respectively. RESULTS: OGD induced apoptosis and suppressed survival in rat hippocampal neurons. And the expression levels of miR-323 were increased after OGD treatment. Furthermore, the up-regulation of miR-323 promoted apoptosis and suppressed survival, whereas the inhibition of miR-323 suppressed apoptosis and enhanced survival in OGD-treated neurons. Moreover, miR-323 could directly bind to BRI3 3'-UTR. Notably, the knockdown of BRI3 by BRI3 siRNA apparently abrogated cell survival and induced cell apoptosis in rat neurons. CONCLUSION: This study indicated that miR-323 might regulate ischemia/reperfusion-induced rat neuronal cell death via targeting BRI3.
PURPOSE:MicroRNA-323 (miR-323) has been reported to be upregulated in Ischemia/Reperfusion (I/R) injury-treated neuronal cell. However, the effect and underlying mechanism of miR-323 in I/R-induced neuronal cell death remains poorly understood. The current study was aim to investigate the role and molecular basis of miR-323 in I/R-induced neuronal cell. METHODS: An oxygen-glucose deprivation (OGD) model of hippocampal neuron I/R was produced in vitro. Cell apoptosis, cell survival, and the expression of miR-323 were determined after 6 h, 12 h and 24 h after OGD treatment. The up- or down-regulation of miR-323 was performed by miR-323 mimics or anti-miR-323, respectively. RESULTS: OGD induced apoptosis and suppressed survival in rat hippocampal neurons. And the expression levels of miR-323 were increased after OGD treatment. Furthermore, the up-regulation of miR-323 promoted apoptosis and suppressed survival, whereas the inhibition of miR-323 suppressed apoptosis and enhanced survival in OGD-treated neurons. Moreover, miR-323 could directly bind to BRI3 3'-UTR. Notably, the knockdown of BRI3 by BRI3 siRNA apparently abrogated cell survival and induced cell apoptosis in rat neurons. CONCLUSION: This study indicated that miR-323 might regulate ischemia/reperfusion-induced ratneuronal cell death via targeting BRI3.
Authors: W Deleersnijder; G Hong; R Cortvrindt; C Poirier; P Tylzanowski; K Pittois; E Van Marck; J Merregaert Journal: J Biol Chem Date: 1996-08-09 Impact factor: 5.157
Authors: Kira S Sheinerman; Jon B Toledo; Vladimir G Tsivinsky; David Irwin; Murray Grossman; Daniel Weintraub; Howard I Hurtig; Alice Chen-Plotkin; David A Wolk; Leo F McCluskey; Lauren B Elman; John Q Trojanowski; Samuil R Umansky Journal: Alzheimers Res Ther Date: 2017-11-09 Impact factor: 6.982