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MicroRNA-132 protects hippocampal neurons against oxygen-glucose deprivation-induced apoptosis
Zu-Zhen Sun1, Zhan-Yun Lv1, Wen-Jing Tian1
1Department of Neurology, Affiliated Hospital of Jining Medical University, Jining, China.
Abstract:
Hypoxic-ischemic brain injury (HIBI) results in death or long-term neurologic impairment in both adults and children. In this study, we investigated the effects of microRNA-132 (miR-132) dysregulation on oxygen-glucose deprivation (OGD)-induced apoptosis in fetal rat hippocampal neurons, in order to reveal the therapeutic potential of miR-132 on HIBI. MiR-132 dysregulation was induced prior to OGD exposure by transfection of primary fetal rat hippocampal neurons with miR-132 mimic or miR-132 inhibitor. The effects of miR-132 overexpression and suppression on OGD-stimulated hippocampal neurons were evaluated by detection of cell viability, apoptotic cells rate, and the expression of apoptosis-related proteins. Besides, TargetScan database and dual luciferase activity assay were used to seek a target gene of miR-132. As a result, miR-132 was highly expressed in hippocampal neurons following 2 h of OGD exposure. MiR-132 overexpression significantly increased OGD-diminished cell viability and reduced OGD-induced apoptosis at 12, 24, and 48 h post-OGD. MiR-132 overexpression significantly down-regulated the expressions of Bax, cytochrome c, and caspase-9, but up-regulated BCl-2. Caspase-3 activity was also significantly decreased by miR-132 overexpression. Furthermore, FOXO3 was a direct target of miR-132, and it was negatively regulated by miR-132. To conclude, our results provide evidence that miR-132 protects hippocampal neurons against OGD injury by inhibiting apoptosis.
Insights
MicroRNA-132 (miR-132) protects fetal rat hippocampal neurons from oxygen-glucose deprivation (OGD) injury. Upregulating miR-132 enhances cell viability and inhibits apoptosis, suggesting therapeutic potential for hypoxic-ischemic brain injury (HIBI).
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Hypoxic-ischemic brain injury (HIBI) causes severe neurological damage in all age groups.
- MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including apoptosis.
- Dysregulation of specific miRNAs, like miR-132, is implicated in brain injury pathogenesis.
Purpose of the Study:
- To investigate the role of microRNA-132 (miR-132) in oxygen-glucose deprivation (OGD)-induced apoptosis in fetal rat hippocampal neurons.
- To explore the therapeutic potential of modulating miR-132 levels for treating HIBI.
Main Methods:
- Primary fetal rat hippocampal neurons were transfected with miR-132 mimic or inhibitor before OGD exposure.
- Cell viability, apoptosis rates, and expression of apoptosis-related proteins (Bax, cytochrome c, caspase-9, BCl-2, caspase-3) were assessed.
- The TargetScan database and dual luciferase assay were used to identify and validate miR-132 targets.
Main Results:
- miR-132 expression was upregulated in hippocampal neurons after OGD exposure.
- Overexpression of miR-132 significantly improved cell viability and reduced apoptosis following OGD.
- miR-132 overexpression altered the expression of key apoptosis regulators, including downregulating Bax, cytochrome c, and caspase-9, and upregulating BCl-2.
- FOXO3 was identified as a direct target negatively regulated by miR-132.
Conclusions:
- miR-132 exhibits a protective effect against OGD-induced injury in hippocampal neurons.
- The findings suggest that miR-132 exerts its neuroprotective effects by inhibiting apoptosis through the regulation of FOXO3 and other apoptosis-related proteins.
- Modulating miR-132 presents a potential therapeutic strategy for HIBI.
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