JOURNAL ARTICLE

MiR-340-5p alleviates oxygen-glucose deprivation/reoxygenation-induced neuronal injury via PI3K/Akt activation by targeting PDCD4

Yake Zheng, Peng Zhao, Yajun Lian, Shuang Li, Yuan Chen, Lihao Li
Neurochemistry International 2019 December 20, : 104650
31870893
MicroRNA-340-5p (miR-340-5p), a suppressor of certain target genes in brain, reportedly is decreased in peripheral circulation of acute stroke patients. However, little is known regarding its role in regulating cerebral ischemia/reperfusion injury. This study explores the effect of miR-340-5p on ischemia/reperfusion insults by exposing rat hippocampal neurons to oxygen-glucose deprivation/reoxygenation (OGDR) in vitro. We found miR-340-5p to be poorly expressed in these neurons after OGDR stimulation. OGDR stimulation decreased cell viability, increased lactate dehydrogenase (LDH) activity and cell apoptosis, all of which were significantly inhibited by miR-340-5p overexpression and enhanced by miR-340-5p inhibition. Using bioinformatics analysis, we identified mRNA encoding the pro-apoptotic factor, programmed cell death 4 (PDCD4) as a putative target of miR-340-5p. A dual-luciferase reporter assay suggested that miR-340-5p targeted the 3'-UTR of PDCD4. PDCD4 was upregulated in cells exposed to OGDR, and miR-340-5p negatively modulated expression of PDCD4. PDCD4 overexpression partly reversed the neuroprotective effect of miR-340-5p during OGDR-induced injury. MiR-340-5p overexpression significantly promoted the activation of PI3K/Akt signaling pathway (P < 0.05) in OGDR-exposed cells, and PDCD4 overexpression attenuated this effect (P < 0.05). Collectively, our results indicate that miR-340-5p might exerted neuroprotective effects during OGDR injury by targeting PDCD4 and then activating the PI3K/Akt pathway. These results indicated a novel target for treating cerebral ischemic injury.

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