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ΜicroRNA-122 protects against ischemic stroke by targeting Maf1
Mengmeng Wang1, Xiaoman Liu1, Yu Wu2
1Department of Neurology, Affiliated Xinhua Hospital of Dalian University, Dalian, Liaoning 116021, P.R. China.
Abstract:
The protection of brain tissue against damage and the reduction of infarct size is crucial for improving patient prognosis following ischemic stroke. Therefore, the present study aimed to investigate the regulatory effect of microRNA (miR)-122 and its target gene repressor of RNA polymerase III transcription MAF1 homolog (Maf1) on the infarct area in ischemic stroke. Reverse transcription-quantitative PCR (RT-qPCR) was performed to determine miR-122 expression levels in an ischemic stroke [middle cerebral artery occlusion (MCAO)] mouse model. Nissl staining was conducted to measure the infarct area of the MCAO mouse model. Moreover, RT-qPCR was performed to investigate the relationship between the expression of Maf1 and miR-122 in the MCAO mouse model. Dual-luciferase reporter assay in vitro and miR-122 mimic or inhibitor treatment in vivo were conducted to verify that miR-122 targeted and inhibited Maf1 expression. The results suggested that miR-122 was upregulated in the brain tissue of MCAO model mice. miR-122 overexpression effectively reduced the size of the infarct area in comparison with a control and miR-122 knockdown in brain tissue resulted in the opposite effect. Moreover, Maf1 was confirmed to be a direct target of miR-122. The results of a dual-luciferase reporter assay indicated that miR-122 bound to the 3'-untranslated region of Maf1. Maf1 expression decreased after stroke model induction in comparison with that in sham animals, and Maf1 expression was negatively associated with the expression of miR-122. In addition, miR-122 knockdown increased Maf1 expression levels, whereas miR-122 overexpression decreased Maf1 expression levels in comparison with a control. In conclusion, the results suggested that miR-122 improved the outcome of acute ischemic stroke by reducing the expression of Maf1.
Insights
MicroRNA-122 (miR-122) protects brain tissue after ischemic stroke by downregulating MAF1. Upregulated miR-122 reduces infarct size, improving outcomes in stroke models.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Ischemic stroke poses significant risks to brain tissue, necessitating strategies to reduce damage and infarct size.
- MicroRNAs (miRNAs) play critical roles in post-transcriptional gene regulation, influencing various cellular processes.
- Understanding the molecular mechanisms underlying stroke pathology is vital for developing effective therapeutic interventions.
Purpose of the Study:
- To investigate the regulatory role of microRNA-122 (miR-122) and its target gene, MAF1 homolog (Maf1), in ischemic stroke.
- To determine the effect of miR-122 on infarct area and brain tissue protection in a middle cerebral artery occlusion (MCAO) mouse model.
- To elucidate the interaction between miR-122 and Maf1 expression in the context of ischemic stroke.
Main Methods:
- Establishment of an ischemic stroke model using middle cerebral artery occlusion (MCAO) in mice.
- Quantitative reverse transcription PCR (RT-qPCR) to measure miR-122 and Maf1 expression levels.
- Nissl staining to quantify infarct area.
- Dual-luciferase reporter assay to confirm direct targeting of Maf1 by miR-122.
- In vivo administration of miR-122 mimic or inhibitor to assess functional effects.
Main Results:
- miR-122 expression was significantly upregulated in the brain tissue of MCAO mice.
- Overexpression of miR-122 reduced infarct size, while miR-122 knockdown increased it.
- Maf1 was identified as a direct target of miR-122, with its expression decreasing post-stroke and negatively correlating with miR-122 levels.
- miR-122 inhibition led to increased Maf1 expression, whereas miR-122 overexpression decreased Maf1 expression.
Conclusions:
- miR-122 plays a protective role in acute ischemic stroke by inhibiting Maf1 expression.
- The miR-122/Maf1 axis represents a potential therapeutic target for improving outcomes in ischemic stroke.
- Modulating miR-122 levels could offer a novel strategy for neuroprotection following stroke.
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