Abstract | BACKGROUND AND PURPOSE: We previously showed that the microRNA miR-424 protects against permanent cerebral ischemic injury in mice by suppressing microglia activation. This study investigated the role of miR-424 in transient cerebral ischemia in mice with a focus on oxidative stress-induced neuronal injury. METHODS: RESULTS: MiR-424 levels in the peri- infarct cortex increased at 1 and 4 hours then decreased 24 hours after reperfusion. Treatment with miR-424 decreased infarct volume and inhibited neuronal apoptosis after ischemia/reperfusion, reduced reactive oxygen species and malondialdehyde levels in the cortex, and increased the expression and activation of MnSOD as well as the expression of extracellular SOD and the redox-sensitive transcription factor nuclear factor erythroid 2-related factor. In neuronal cultures, miR-424 treatment abrogated H2O2-induced injury, as evidenced by decreased lactate dehydrogenase leakage and malondialdehyde level and increased cell viability and MnSOD activity; the protective effects of miR-424 against oxidative stress were reversed by nuclear factor erythroid 2-related factor knockdown and SOD inhibitor treatment. CONCLUSIONS:
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Authors | Ping Liu, Haiping Zhao, Rongliang Wang, Peng Wang, Zhen Tao, Li Gao, Feng Yan, Xiangrong Liu, Shun Yu, Xunming Ji, Yumin Luo |
Journal | Stroke
(Stroke)
Vol. 46
Issue 2
Pg. 513-9
(Feb 2015)
ISSN: 1524-4628 [Electronic] United States |
PMID | 25523055
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2014 American Heart Association, Inc. |
Chemical References |
- MIRN424 microRNA, mouse
- MicroRNAs
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Topics |
- Animals
- Brain Ischemia
(metabolism, pathology, prevention & control)
- Cells, Cultured
- Cerebral Cortex
(metabolism, pathology)
- Male
- Mice
- Mice, Inbred C57BL
- MicroRNAs
(biosynthesis)
- Oxidative Stress
(physiology)
- Reperfusion Injury
(metabolism, pathology, prevention & control)
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