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      miR-497 regulates neuronal death in mouse brain after transient focal cerebral ischemia

      , , , , , ,
      Neurobiology of Disease
      Elsevier BV

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          Abstract

          Dysfunction of the microRNA (miR) network has been emerging as a major regulator in neurological diseases. However, little is known about the functional significance of unique miRs in ischemic brain damage. Here, we found that miR-497 is induced in mouse brain after transient middle cerebral artery occlusion (MCAO) and mouse N2A neuroblastoma (N2A) cells after oxygen-glucose deprivation (OGD). Loss-of-miR-497 function significantly suppresses OGD-induced N2A cell death, whereas gain-of-miR-497 function aggravates OGD-induced neuronal loss. Moreover, miR-497 directly binds to the predicted 3'-UTR target sites of bcl-2/-w genes. Furthermore, knockdown of cerebral miR-497 effectively enhances bcl-2/-w protein levels in the ischemic region, attenuates ischemic brain infarction, and improves neurological outcomes in mice after focal cerebral ischemia. Taken together, our data suggest that miR-497 promotes ischemic neuronal death by negatively regulating antiapoptotic proteins, bcl-2 and bcl-w. We raise the possibility that this pathway may contribute to the pathogenesis of the ischemic brain injury in stroke. Copyright 2009 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          Neurobiology of Disease
          Neurobiology of Disease
          Elsevier BV
          09699961
          April 2010
          April 2010
          : 38
          : 1
          : 17-26
          Article
          10.1016/j.nbd.2009.12.021
          2837803
          20053374
          9242825c-6930-4ff7-a9be-0c82c4a8670d
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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