MicroRNA-365 Knockdown Prevents Ischemic Neuronal Injury by Activating Oxidation Resistance 1-Mediated Antioxidant Signals

【Author】

Jia-Lin Mo;Zhi-Guang Pan;Xiao Chen;Yu Lei;Ling-Ling Lv;Cheng Qian;Feng-Yan Sun;Department of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences,Fudan University;State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University;Department of Neurosurgery, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University;Shanghai Key Laboratory of Clinical Geriatric Medicine,Research Center on Aging and Medicine, Shanghai Medical College, Fudan University;

【Institution】

Department of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences,Fudan University;State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University;Department of Neurosurgery, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University;Shanghai Key Laboratory of Clinical Geriatric Medicine,Research Center on Aging and Medicine, Shanghai Medical College, Fudan University;

【Abstract】

Micro RNA-365(mi R-365) is upregulated in the ischemic brain and is involved in oxidative damage in the diabetic rat. However, it is unclear whether mi R-365 regulates oxidative stress(OS)-mediated neuronal damage after ischemia. Here, we used a transient middle cerebral artery occlusion model in rats and the hydrogen peroxide-induced OS model in primary cultured neurons to assess the roles of mi R-365 in neuronal damage. We found that mi R-365 exacerbated ischemic brain injury and OS-induced neuronal damage and was associated with a reduced expression of OXR1(Oxidation Resistance 1). In contrast, mi R-365 antagomir alleviated both the brain injury and OXR1 reduction. Luciferase assays indicated that mi R-365 inhibited OXR1 expression by directly targeting the 30-untranslated region of Oxr1. Furthermore, knockdown of OXR1 abolished the neuroprotective and antioxidant effects of the mi R-365 antagomir. Our results suggest that mi R-365 upregulationincreases oxidative injury by inhibiting OXR1 expression,while its downregulation protects neurons from oxidative death by enhancing OXR1-mediated antioxidant signals.

【Keywords】

MicroRNA;;Ischemic stroke;;Neuronal damage;;Oxidative stress;;Neuroprotection

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