miR-374 improves cerebral ischemia reperfusion injury by targeting Wnt5a
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 inj...
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| Published in | Experimental Animals Vol. 70; no. 1; pp. 126 - 136 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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Japan
Japanese Association for Laboratory Animal Science
01.01.2021
Japan Science and Technology Agency |
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| 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. |
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| AbstractList | 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. 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. |
| Author | Liu, Yongrong Dong, Ruifang Xing, Fangyuan Cheng, Ye |
| Author_xml | – sequence: 1 fullname: Xing, Fangyuan organization: Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei 061000, People’s Republic of China – sequence: 2 fullname: Liu, Yongrong organization: Department of Ultrasound, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei 061000, People’s Republic of China – sequence: 3 fullname: Dong, Ruifang organization: Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei 061000, People’s Republic of China – sequence: 4 fullname: Cheng, Ye organization: Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, Hebei 061000, People’s Republic of China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33116025$$D View this record in MEDLINE/PubMed |
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| Keywords | reperfusion injury brain ischemia Wnt5a miR-374 |
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| References_xml | – reference: 17. Nemeth MJ, Topol L, Anderson SM, Yang Y, Bodine DM. Wnt5a inhibits canonical Wnt signaling in hematopoietic stem cells and enhances repopulation. Proc Natl Acad Sci USA. 2007; 104: 15436–15441. – reference: 20. Blumenthal A, Ehlers S, Lauber J, Buer J, Lange C, Goldmann T, et al. The Wingless homolog WNT5A and its receptor Frizzled-5 regulate inflammatory responses of human mononuclear cells induced by microbial stimulation. Blood. 2006; 108: 965–973. – reference: 26. Halleskog C, Dijksterhuis JP, Kilander MB, Becerril-Ortega J, Villaescusa JC, Lindgren E, et al. Heterotrimeric G protein-dependent WNT-5A signaling to ERK1/2 mediates distinct aspects of microglia proinflammatory transformation. J Neuroinflammation. 2012; 9: 111. – reference: 13. van Amerongen R, Mikels A, Nusse R. Alternative wnt signaling is initiated by distinct receptors. Sci Signal. 2008; 1: re9. – reference: 18. Kumawat K, Gosens R. WNT-5A: signaling and functions in health and disease. Cell Mol Life Sci. 2016; 73: 567–587. – reference: 11. Zhang SB, Liu TJ, Pu GH, Li BY, Gao XZ, Han XL. MicroRNA-374 Exerts Protective Effects by Inhibiting SP1 Through Activating the PI3K/Akt Pathway in Rat Models of Myocardial Ischemia-Reperfusion After Sevoflurane Preconditioning. Cell Physiol Biochem. 2018; 46: 1455–1470. – reference: 38. Puig B, Brenna S, Magnus T. Molecular Communication of a Dying Neuron in Stroke. Int J Mol Sci. 2018; 19: 19. – reference: 9. Kim T, Mehta SL, Morris-Blanco KC, Chokkalla AK, Chelluboina B, Lopez M, et al. The microRNA miR-7a-5p ameliorates ischemic brain damage by repressing α-synuclein. Sci Signal. 2018; 11: eaat4285. – reference: 19. McDonald SL, Silver A. The opposing roles of Wnt-5a in cancer. Br J Cancer. 2009; 101: 209–214. – reference: 28. Peña ID, Borlongan C, Shen G, Davis W. Strategies to Extend Thrombolytic Time Window for Ischemic Stroke Treatment: An Unmet Clinical Need. J Stroke. 2017; 19: 50–60. – reference: 5. Hu Y, Deng H, Xu S, Zhang J. MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury. Int J Mol Sci. 2015; 16: 24895–24917. – reference: 27. Ding S, Xu Z, Yang J, Liu L, Huang X, Wang X, et al. The Involvement of the Decrease of Astrocytic Wnt5a in the Cognitive Decline in Minimal Hepatic Encephalopathy. Mol Neurobiol. 2017; 54: 7949–7963. – reference: 36. Jung YS, Oh AY, Park HP, Hwang JW, Lim YJ, Jeon YT. Post-ischemic administration of pravastatin reduces neuronal injury by inhibiting Bax protein expression after transient forebrain ischemia in rats. Neurosci Lett. 2015; 594: 87–92. – reference: 10. Liu FJ, Lim KY, Kaur P, Sepramaniam S, Armugam A, Wong PT, et al. microRNAs Involved in Regulating Spontaneous Recovery in Embolic Stroke Model. PLoS One. 2013; 8: e66393. – reference: 29. Datta A, Sarmah D, Mounica L, Kaur H, Kesharwani R, Verma G, et al. Cell Death Pathways in Ischemic Stroke and Targeted Pharmacotherapy. Transl Stroke Res. 2020; 11: 1185–1202. – reference: 39. Zhang P, Yang L, He H, Deng Y. Differential variations of autophagy and apoptosis in permanent focal cerebral ischaemia rat model. Brain Inj. 2017; 31: 1151–1158. – reference: 31. Patel RAG, McMullen PW. Neuroprotection in the Treatment of Acute Ischemic Stroke. Prog Cardiovasc Dis. 2017; 59: 542–548. – reference: 21. Ouchi N, Higuchi A, Ohashi K, Oshima Y, Gokce N, Shibata R, et al. Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity. Science. 2010; 329: 454–457. – reference: 33. He CW, Liao CP, Pan CL. Wnt signalling in the development of axon, dendrites and synapses. Open Biol. 2018; 8: 8. – reference: 2. Banerjee S, Williamson D, Habib N, Gordon M, Chataway J. Human stem cell therapy in ischaemic stroke: a review. Age Ageing. 2011; 40: 7–13. – reference: 25. Zhang W, Wang Y, Bi G. 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| Snippet | To date, studies have demonstrated the potential functions of microRNAs in cerebral ischemia reperfusion (IR) injury. Herein, we established a middle cerebral... To date, studies have demonstrated the potential functions of microRNAs in cerebral ischemia reperfusion (IR) injury. Herein, we established a middle cerebral... |
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| SubjectTerms | Animals Apoptosis Bcl-2 protein Bcl-x protein bcl-X Protein - genetics bcl-X Protein - metabolism Blood-brain barrier Brain damage Brain injury brain ischemia Brain Ischemia - etiology Brain Ischemia - genetics Brain Ischemia - therapy Cerebral blood flow Cerebral infarction Disease Models, Animal Down-Regulation - drug effects Edema Gene expression Gene Expression - genetics Head injuries Infarction Infarction, Middle Cerebral Artery - complications Infarction, Middle Cerebral Artery - genetics Ischemia Male MicroRNAs MicroRNAs - metabolism MicroRNAs - pharmacology MicroRNAs - physiology MicroRNAs - therapeutic use miR-374 miRNA Molecular Targeted Therapy Occlusion Original Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Rats, Sprague-Dawley Reperfusion reperfusion injury Reperfusion Injury - complications Reperfusion Injury - genetics Ribonucleic acid RNA Wnt protein Wnt-5a Protein - genetics Wnt-5a Protein - metabolism Wnt5a |
| Title | miR-374 improves cerebral ischemia reperfusion injury by targeting Wnt5a |
| URI | https://www.jstage.jst.go.jp/article/expanim/70/1/70_20-0034/_article/-char/en https://www.ncbi.nlm.nih.gov/pubmed/33116025 https://www.proquest.com/docview/2494935113 https://pubmed.ncbi.nlm.nih.gov/PMC7887619 |
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