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Updated: Oct 27, 2025
A Simple Alternative to Stereotactic Injection for Brain Specific Knockdown of miRNA
Published on: December 26, 2015
MiR-125a-5p silencing inhibits cerebral ischemia-induced injury through targeting IGFBP3
Bo Song1, Jing Xu1, Ping Zhong1
1Department of Neurology, Qingdao Central Hospital, Qingdao, Shandong, China.
Abstract:
Dysregulated microRNAs (miRNAs) are crucial regulators of cerebrovascular conditions, including ischemic stroke. Circulating miR-125a-5p is associated with ischemic stroke and may have clinical utility as an early diagnostic biomarker. This study conducted a series of experiments that were designed to elucidate the regulatory action of miR-125a-5p in ischemic brain injury and its underlying mechanisms. The results of this study found that the expression of miR-125a-5p was increased in BV2 microglial cells under oxygen-glucose deprivation/reoxygenation (OGD/R) setting, as well as in rat brain tissue after middle cerebral artery occlusion (MCAO). OGD/R triggered BV2 microglial cell apoptosis, whereas downregulation of miRNA-125a-5p suppressed the apoptosis rate in OGD/R-induced BV2 microglial cells. Subsequently, insulin-like growth factor binding protein 3 (IGFBP3) is a molecular target of miR-125a-5p, and IGFBP3 knockdown reversed the effects of miR-125a-5p inhibitor on BV2 microglial cells in vitro. These data supported the fact that miR-125a-5p silencing protects against cerebral ischemia-induced injury by targeting IGFBP3.
Insights
MicroRNA-125a-5p (miR-125a-5p) is upregulated in ischemic stroke. Silencing miR-125a-5p protects against brain injury by targeting insulin-like growth factor binding protein 3 (IGFBP3).
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) play a role in cerebrovascular diseases like ischemic stroke.
- Circulating miR-125a-5p is linked to ischemic stroke and shows potential as an early diagnostic biomarker.
Purpose of the Study:
- To investigate the regulatory role of miR-125a-5p in ischemic brain injury.
- To elucidate the mechanisms underlying miR-125a-5p's action in cerebral ischemia.
Main Methods:
- Examined miR-125a-5p expression in BV2 microglial cells under oxygen-glucose deprivation/reoxygenation (OGD/R) and in rat brain tissue after middle cerebral artery occlusion (MCAO).
- Assessed the impact of miR-125a-5p downregulation on OGD/R-induced BV2 microglial cell apoptosis.
- Identified and validated insulin-like growth factor binding protein 3 (IGFBP3) as a molecular target of miR-125a-5p.
Main Results:
- miR-125a-5p expression increased in BV2 cells and rat brains following ischemic conditions (OGD/R and MCAO).
- Downregulating miR-125a-5p reduced apoptosis in OGD/R-treated BV2 cells.
- Knockdown of IGFBP3 counteracted the protective effects of miR-125a-5p inhibition in vitro.
Conclusions:
- miR-125a-5p silencing confers protection against cerebral ischemia-induced injury.
- The protective mechanism involves targeting insulin-like growth factor binding protein 3 (IGFBP3).
- miR-125a-5p emerges as a potential therapeutic target for ischemic stroke.
