MiR-455-5p Attenuates Cerebral Ischemic Reperfusion Injury by Targeting FLT3.
J Cardiovasc Pharmacol
; 76(5): 627-634, 2020 11.
Article
em En
| MEDLINE
| ID: mdl-32833902
ABSTRACT
Cerebral ischemia-reperfusion (I/R) injury is a terrible disease which results in the dysfunction and structural damage of brain tissues. Growing evidence implies that miR-455-5p is implicated in the regulation of pathogenesis of several diseases. The aim of this study is to reveal the role of miR-455-5p in cerebral I/R injury and the regulatory mechanism. We established a vitro model by inducing SH-SY5Y and PC-12 cells with oxygen-glucose deprivation and reoxygenation. The experimental cerebral I/R rat model was established by middle cerebral artery occlusion operation. The findings indicated that miR-455-5p expression was downregulated in oxygen-glucose deprivation and reoxygenation induced cells and I/R rat model. In addition, miR-455-5p upregulation inhibited SH-SY5Y cell apoptosis and cerebral damage, whereas miR-455-5p silencing promoted SH-SY5Y cell apoptosis and cerebral damage. Mechanistically, luciferase reporter assay corroborated that miR-455-5p could bind with feline mcDonough sarcoma-like tyrosine kinase 3 (FLT3) mRNA. However, the role of FLT3 in cerebral I/R injury was rarely investigated. Real-time polymerase chain reaction revealed that FTL3 expression was negatively regulated by miR-455-5p. FTL3 upregulation reversed the inhibitory effects of miR-455-5p upregulation on PC-12 and SH-SY5Y cell apoptosis. Therefore, our study verified that miR-455-5p improved cerebral I/R injury by targeting FLT3, which suggests a potential new target for the prevention of cerebral I/R injury.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Encéfalo
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Traumatismo por Reperfusão
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Infarto da Artéria Cerebral Média
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MicroRNAs
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Tirosina Quinase 3 Semelhante a fms
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Neurônios
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Humans
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Male
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article