Inhibition of miR-497 improves functional outcome after ischemic stroke by enhancing neuronal autophagy in young and aged rats

Xudong Chen, Siyang Lin, Lei Gu, Xiaohong Zhu, Yinuo Zhang, Hongxia Zhang, Bei Shao, Qichuan Zhuge, Kunlin Jin

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

Over the years miR-497 has been found to play a vital role in the pathogenesis of neurological diseases, including ischemic stroke. However, its underlying mechanism remains largely unexplored. Here, we used miR-497 agomir (miR-497 agonist), miR-497 antagomir (miR-497 inhibitor) and 3-MA (autophagy inhibitor) to treat ischemic rats (n = 10–12 per group) induced by permanent distal middle cerebral artery occlusion (dMCAO), followed the functional outcome assessment 24 h after dMCAO. We found that treatment of miR-497 antagomir, but not miR-497 angomir, reduced the infarct volume and improved neurological deficits after ischemic stroke, along with upregulation of the autophagy-related protein LC3 expression (mean ± SEM,p < 0.05). While the ischemic rats treated with 3-MA exhibited inhibition of autophagy, which in turn abolished functional recovery as observed in miR-497 antagomir-treated group (p < 0.05). Interestingly, the role of miR-497 in functional recovery in aged ischemic rats was less effective, compared to young adult ischemic rats (p < 0.05). Our data suggest that inhibition of miR-497 could protect cerebral ischemic injury by enhancing autophagy and also age-dependent.

Original languageEnglish
Pages (from-to)64-72
Number of pages9
JournalNeurochemistry International
Volume127
DOIs
StatePublished - Jul 2019

Keywords

  • Aging
  • Autophagy
  • Ischemic stroke
  • MiRNA
  • Neuroprotection
  • miR-497

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