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Year : 2021  |  Volume : 69  |  Issue : 6  |  Page : 1601--1607

MiR-191-5p Disturbed the Angiogenesis in a Mice Model of Cerebral Infarction by Targeting Inhibition of BDNF

1 Department of Neurology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, 646000, China
2 Department of Orthopedics, Luzhou People's Hospital, Luzhou, 646000, China

Correspondence Address:
Dr. Sijin Yang
Department of Neurology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, No.182 Chunhui Road, Longmatan District, Luzhou, SiChuan, 646000
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.333459

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Background: miRNAs are crucial regulators of angiogenesis, but there have been no detailed studies on the role of miR-191-5p in cerebral infarct angiogenesis. Here, we investigated the role of miR-191-5p in regulating cerebral infarction angiogenesis. Material and Methods: Mice were injected intracerebroventricularly with antagomir negative control (NC-antagomir), miR-191-5p antagomir, or pcDNA-BDNF 2 h before middle cerebral artery occlusion (MCAO), followed by neurobehavioral score and foot-fault test. The cerebral infarct volume was performed by TTC staining. The microvessel density was detected by FITC-dextran. RT-qPCR was used to detect the levels of miR-191-5p and its target gene BDNF. Western blotting was applied to detect the protein levels of BDNF. The luciferase reporter assay verified that miR-191-5p targeted BDNF. Results: We found an increased level of miR-191-5p in the brain tissue of mice to MCAO. Down-regulation of miR-191-5p reduced the infarct volume and ameliorated neurological deficits in MCAO mice. Further investigation showed that miR-191-5p directly targeted BDNF and that the protective effect of miR-191-5p inhibition in angiogenesis was achieved by regulating BDNF. Conclusions: Our results indicated that miR-191-5p disturbed the angiogenesis in the mouse models of cerebral infarction by inhibiting BDNF.


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Online since 20th March '04
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