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Published on: July 14, 2016
Runx1 promotes neuronal injury in ischemic stroke through mediating miR-203-3p/Pde4d axis
1Department of Neurosurgery, Hunan Provincial People's Hospital (The first affiliated hospital of Hunan normal university), Changsha, Hunan, P.R. China.
Background:
It has been reported that Runx1 engaged in IS progression, but the detailed mechanism of Runx1 in IS is still unclear.
Methods:
Mice and HT22 cells were subjected to the process of middle cerebral artery occlusion and reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R), respectively. Infract volume was tested using TTC staining. The levels of inflammatory cytokines were investigated using ELISA assay. Cell viability was examined utilizing MTS. Apoptosis rate was evaluated using flow cytometry and TUNEL. The productions of SOD and MDA were monitored by means of commercial kits. The correlations among Runx1, miR-203-3p and Pde4d were ascertained using dual luciferase reporter gene, ChIP and RNA-RNA pull-down assays.
Results:
Runx1 and Pde4d were abnormally elevated, while miR-203-3p was notably declined in MCAO/R mice and OGD/R-induced HT22 cells. OGD/R treatment suppressed cell viability and facilitated cell apoptosis, inflammation and oxidative stress, which were compromised by Runx1 knockdown or miR-203-3p upregulation. Runx1 bound to miR-203-3p promoter, thus decreasing miR-203-3p expression. MiR-203-3p inhibited Pde4d expression via targeting Pde4d mRNA. Runx1 deficiency-induced protection effects on OGD/R-treated HT22 cells were offset by miR-203-3p downregulation.
Conclusion:
Runx1 aggravated neuronal injury caused by IS through mediating miR-203-3p/Pde4d axis.
Insights
Runx1 exacerbates ischemic stroke (IS) injury by suppressing miR-203-3p, which normally inhibits Pde4d. This study clarifies the Runx1-miR-203-3p-Pde4d pathway in IS progression.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Runx1 is implicated in ischemic stroke (IS) progression.
- The precise molecular mechanisms of Runx1 in IS remain incompletely understood.
Purpose of the Study:
- To elucidate the role and mechanism of Runx1 in ischemic stroke (IS).
- To investigate the regulatory axis involving Runx1, miR-203-3p, and Pde4d in neuronal injury.
Main Methods:
- Middle cerebral artery occlusion and reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in HT22 cells were employed.
- Infarct volume, inflammatory cytokines, cell viability, apoptosis, and oxidative stress markers (SOD, MDA) were assessed.
- Dual luciferase reporter, ChIP, and RNA-RNA pull-down assays were used to determine molecular interactions.
Main Results:
- Runx1 and Pde4d were upregulated, while miR-203-3p was downregulated in IS models.
- OGD/R impaired cell viability and increased apoptosis, inflammation, and oxidative stress.
- Runx1 suppressed miR-203-3p expression by binding to its promoter, and miR-203-3p inhibited Pde4d.
- Runx1 knockdown or miR-203-3p upregulation mitigated OGD/R-induced damage, while miR-203-3p downregulation offset Runx1 deficiency protection.
Conclusions:
- Runx1 aggravates neuronal injury in ischemic stroke (IS) by regulating the miR-203-3p/Pde4d axis.
- Targeting the Runx1-miR-203-3p-Pde4d pathway may offer therapeutic potential for IS.
