Journal
NEUROSCIENCE LETTERS
Volume 662, Issue -, Pages 233-241Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2017.10.046
Keywords
MicroRNA-215; Nuclear factor activator 1; Middle cerebral artery occlusion; Ischemic injury
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Funding
- National Natural Science Foundation of China [81471204]
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Objective: This study investigated the role of miR-215 and nuclear factor-KB activator (Act)1 and their mechanisms of action in ischemic stroke. Methods: Cell viability was examined with the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay; cell apoptosis was detected by flow cytometry; and mRNA and protein expression was assessed by quantitative real-time PCR and western blotting, respectively. A mouse model of middle cerebral artery occlusion (MCAO) was treated with or without miR-215 mimic to verify the in vitro results. The relationship between miR-215 and interleukin (IL)-17 was evaluated in human peripheral blood from 29 patients. Results: Actl was upregulated whereas miR-215 was downregulated in ischemic stroke. Overexpression of miR-215 by transfection of a mimic repressed Actl protein levels in vitro and in vivo, although the luciferase assay showed that miR-215 did not directly bind to the 3' untranslated region of Actl. MiR-215 overexpression inhibited cell apoptosis and autophagy. Increasing miR-215 levels reduced ischemic infarction and improved neurological deficit, while loss of miR-215 phenocopied the effects of IL -17. Conclusion: Upregulation of miR-215 exerts neuroprotection against ischemic injury by negatively regulating Act1/IL-17 receptor A signaling. These findings provide potential therapeutic targets for the treatment of ischemic stroke.
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