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miR-374 improves cerebral ischemia reperfusion injury by targeting Wnt5a
Fangyuan Xing1, Yongrong Liu2, Ruifang Dong1
1Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei 061000, People's Republic of China.
Abstract:
To date, studies have demonstrated the potential functions of microRNAs in cerebral ischemia reperfusion (IR) injury. Herein, we established a middle cerebral artery occlusion (MCAO) model in rats and then subjected them to reperfusion to explore the role of microRNA-374 (miR-374) in cerebral IR injury. After reperfusion, the endogenous miR-374 level decreased, and the expression of its target gene, Wnt5a, increased in brain tissues. Intracerebral pretreatment of miR-374 agomir attenuated cerebral damage induced by IR, including neurobehavioral deficits, infarction, cerebral edema and blood-brain barrier disruption. Moreover, rats pretreated with miR-374 agomir showed a remarkable decrease in apoptotic neurons, which was further confirmed by reduced BAX expression as well as increased BCL-2 and BCL-XL expression. A dual-luciferase reporter assay substantiated that Wnt5a was the target gene of miR-374. miR-374 might protect against brain injury by downregulating Wnt5a in rats after IR. Thus, our study provided a novel mechanism of cerebral IR injury from the perspective of miRNA regulation.
Insights
MicroRNA-374 (miR-374) protects against brain injury following cerebral ischemia reperfusion (IR). Upregulating miR-374 in rats reduced damage by targeting the Wnt5a gene.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play roles in cerebral ischemia reperfusion (IR) injury.
- The specific function of microRNA-374 (miR-374) in this context requires further investigation.
Purpose of the Study:
- To investigate the role of miR-374 in cerebral IR injury using a rat model.
- To elucidate the underlying molecular mechanism involving miR-374 and its target gene, Wnt5a.
Main Methods:
- Established a middle cerebral artery occlusion (MCAO) and reperfusion model in rats.
- Measured miR-374 and Wnt5a expression levels post-reperfusion.
- Administered miR-374 agomir intracerebrally to assess protective effects.
- Evaluated neurobehavioral deficits, infarction, cerebral edema, blood-brain barrier integrity, and apoptosis.
- Utilized a dual-luciferase reporter assay to confirm Wnt5a as a miR-374 target.
Main Results:
- Endogenous miR-374 levels decreased, while Wnt5a expression increased after IR.
- miR-374 agomir pretreatment significantly attenuated IR-induced brain damage and neurobehavioral deficits.
- Apoptotic neuron count decreased, with altered expression of BAX, BCL-2, and BCL-XL.
- Wnt5a was confirmed as a direct target gene of miR-374.
Conclusions:
- miR-374 exerts a protective effect against cerebral IR injury in rats.
- This protection is mediated by the downregulation of its target gene, Wnt5a.
- miRNA regulation offers a novel therapeutic perspective for cerebral IR injury.
