MicroRNA-323 regulates ischemia/reperfusion injury-induced neuronal cell death by targeting BRI3

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...

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Bibliographic Details
Published in:International journal of clinical and experimental pathology 2015-01, Vol.8 (9), p.10725-10733
Main Authors: Yang, Liu, Xiong, Yin, Hu, Xian-Feng, Du, Yan-Hua
Format: Article
Language:English
Subjects:
3' Untranslated Regions
Animals
Animals, Newborn
Apoptosis
Binding Sites
Cell Death
Cell Hypoxia
Cells, Cultured
Gene Expression Regulation
Glucose - deficiency
Hippocampus - metabolism
Hippocampus - pathology
Membrane Proteins - genetics
Membrane Proteins - metabolism
MicroRNAs - genetics
MicroRNAs - metabolism
Nerve Degeneration
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Neurons - metabolism
Neurons - pathology
Original
Oxygen - metabolism
Rats, Sprague-Dawley
Reperfusion Injury - genetics
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Reperfusion Injury - prevention & control
RNA Interference
Time Factors
Transfection
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Summary: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. 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. 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. This study indicated that miR-323 might regulate ischemia/reperfusion-induced rat neuronal cell death via targeting BRI3.
ISSN:1936-2625