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miR-495-3p Attenuates Neuronal Apoptosis Through The Activation of Wnt/MAPK Pathways in Ischemic Stroke
Eunjae Jang1,2, Hee Yu1,3, Jiyun Choi1
1Department of Physiology, Chonnam National University Medical School, Hwasun-Gun, Jeollanamdo, 58128, Republic of Korea.
Abstract:
The incidence of ischemic stroke, involving neuronal cell death and damaged blood vessels, is gradually increasing. In this study, we investigated the effects of a miR-495-3p-I on neuronal viability and recovery using both oxygen-glucose deprivation and recovery (OGD/R) and in transient middle cerebral artery occlusion (tMCAo) models of ischemic stroke. Cell viability increased with miR-495-3p-I treatment compared with the OGD/R group, and both early and late apoptosis decreased through by flow cytometry analysis. In the tMCAo model, tissues injected with miR-495-3p-I showed upregulation of canonical Wnt pathway genes (cyclin D1 and c-Myc) and neuronal marker (Tuj1), while non-canonical Wnt/MAPK pathway genes (caspase-3 and -7) were downregulated. Expression of the pro-apoptotic marker Bax was reduced, whereas the Bcl-2 family protein Mcl-1 increased. Behavioral tests revealed improved motor function compared to the sham group and treatment with miR-495-3p-I reduced brain infarct volume. This research explored the function of miR-495-3p-I in Wnt and MAPK pathways by using the miR-495-3p-I in a model of ischemic stroke, a neurological disease. Thus, we demonstrated that miR-495-3p-I reduced apoptosis and enhanced neuronal cell survival, suggesting it could be a potential therapeutic target.
Insights
MicroRNA-495-3p inhibitor (miR-495-3p-I) enhances neuronal survival and recovery in ischemic stroke models. This study shows miR-495-3p-I reduces apoptosis and improves motor function, suggesting its therapeutic potential.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Ischemic stroke is a growing neurological disease characterized by neuronal cell death and vascular damage.
- MicroRNAs play crucial roles in regulating cellular processes, including survival and apoptosis.
Purpose of the Study:
- To investigate the therapeutic potential of miR-495-3p-I in ischemic stroke models.
- To elucidate the effects of miR-495-3p-I on neuronal viability, apoptosis, and related signaling pathways.
Main Methods:
- Utilized oxygen-glucose deprivation and recovery (OGD/R) and transient middle cerebral artery occlusion (tMCAo) models.
- Assessed cell viability and apoptosis using flow cytometry.
- Analyzed gene and protein expression of Wnt/MAPK pathways and apoptosis markers (Bax, Bcl-2 family).
- Evaluated motor function and brain infarct volume in vivo.
Main Results:
- miR-495-3p-I treatment increased neuronal viability and decreased apoptosis in OGD/R and tMCAo models.
- In tMCAo models, miR-495-3p-I upregulated canonical Wnt pathway genes and neuronal markers while downregulating non-canonical Wnt/MAPK pathway genes.
- miR-495-3p-I reduced pro-apoptotic Bax and increased anti-apoptotic Mcl-1 expression.
- Improved motor function and reduced brain infarct volume were observed in treated animals.
Conclusions:
- miR-495-3p-I demonstrates neuroprotective effects by reducing apoptosis and enhancing neuronal survival in ischemic stroke.
- The mechanism involves modulation of Wnt and MAPK signaling pathways.
- miR-495-3p-I represents a promising therapeutic target for ischemic stroke treatment.
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