Inhibition of miRNA-27b enhances neurogenesis via AMPK activation in a mouse ischemic stroke model.

ABSTRACT: Stroke is a leading cause of death and disability, but treatment options remain limited. Recent studies have suggested that cerebral ischemia-induced neurogenesis plays a vital role in post-stroke repair. Overactivation of AMP-activated protein kinase (AMPK), a master sensor of energy balance, has been reported to exacerbate neuron apoptosis, but the role of chronic AMPK stimulus in post-stroke recovery remains unclear. MicroRNAs have emerged as regulators of neurogenesis and have been reported to be involved in neurological function. In this study, we verified that miR-27b directly targets AMPK and inhibits AMPK expression. In cultured neural stem cells, miR-27b inhibitor improved proliferation and differentiation via the AMPK signaling pathway, but did not have an obvious effect on cell

SUBMITTER: Wang Z 

PROVIDER: S-EPMC6487723 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature