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MiR-455-5p Attenuates Cerebral Ischemic Reperfusion Injury by Targeting FLT3
Jinjing Chen1, Chunran Zhu1, Weijian Jia1
1Department of Neurosurgery, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China; and.
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.
Insights
MicroRNA-455-5p protects against cerebral ischemia-reperfusion injury by targeting FLT3. Upregulating miR-455-5p reduces brain damage and cell apoptosis, offering a potential therapeutic target.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Cerebral ischemia-reperfusion (I/R) injury causes significant brain tissue damage and dysfunction.
- MicroRNA-455-5p (miR-455-5p) is increasingly recognized for its role in various disease pathologies.
- The specific involvement of miR-455-5p in cerebral I/R injury requires elucidation.
Purpose of the Study:
- To investigate the role of miR-455-5p in cerebral I/R injury.
- To identify the underlying regulatory mechanism of miR-455-5p in this context.
Main Methods:
- In vitro models using SH-SY5Y and PC-12 cells subjected to oxygen-glucose deprivation and reoxygenation.
- In vivo cerebral I/R rat model induced by middle cerebral artery occlusion.
- Luciferase reporter assays to confirm direct binding of miR-455-5p to FLT3 mRNA.
- Real-time polymerase chain reaction to assess gene expression levels.
Main Results:
- miR-455-5p expression was significantly downregulated in both in vitro and in vivo cerebral I/R models.
- Upregulation of miR-455-5p demonstrated protective effects, inhibiting cell apoptosis and reducing cerebral damage.
- Silencing miR-455-5p exacerbated cell apoptosis and cerebral damage.
- miR-455-5p directly targets feline mcDonough sarcoma-like tyrosine kinase 3 (FLT3) mRNA.
- FLT3 expression was negatively regulated by miR-455-5p.
- FLT3 upregulation counteracted the protective effects of miR-455-5p in cell apoptosis.
Conclusions:
- miR-455-5p plays a crucial protective role in mitigating cerebral I/R injury.
- The mechanism involves the direct targeting of FLT3 by miR-455-5p.
- miR-455-5p represents a promising therapeutic target for cerebral I/R injury prevention and treatment.
