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Updated: Aug 13, 2026

Endothelin-1 Induced Middle Cerebral Artery Occlusion Model for Ischemic Stroke with Laser Doppler Flowmetry Guidance in Rat
Published on: February 16, 2013
MiR-150 Regulates Poststroke Cerebral Angiogenesis via Vascular Endothelial Growth Factor in Rats
Quan-Wei He1, Qian Li1, Hui-Juan Jin1
1Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Aims:
Angiogenesis is a harmonized target for poststroke recovery. Therefore, exploring the mechanisms involved in angiogenesis after stroke is vitally significant. In this study, we are reporting a miR-150-based mechanism underlying cerebral poststroke angiogenesis.
Methods:
Rat models of middle cerebral artery occlusion (MCAO) and cell models of oxygen-glucose deprivation were conducted. Capillary density, tube formation, cell proliferation, and cell migration were measured by FITC-dextran assay, matrigel assay, Ki-67 staining, and wound healing assay, respectively. The expression of miR-150 and vascular endothelial growth factor (VEGF) was, respectively, measured by RT-PCR and Western blotting. Dual-luciferase assay was conducted to confirm the binding sites between miR-150 and VEGF.
Results:
We found that miR-150 expression in the brain and serum of rats subjected to cerebral ischemia, and in oxygen-glucose-deprived brain microvascular endothelial cells (BMVECs) and astrocytes. Upregulation of miR-150 expression could decrease vascular density of infarct border zone in rat after MCAO and decrease tube formation, proliferation, and migration of BMVECs. We also found that miR-150 could negatively regulate the expression of VEGF, and VEGF was confirmed to be a direct target of miR-150. Moreover, VEGF mediated the function of miR-150 on tube formation, proliferation, and migration of BMVECs.
Conclusions:
Our data suggested that miR-150 could regulate cerebral poststroke angiogenesis in rats through VEGF.
Insights
MicroRNA-150 (miR-150) negatively regulates poststroke angiogenesis by targeting vascular endothelial growth factor (VEGF). This finding reveals a novel mechanism influencing cerebral recovery after stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Cardiovascular Biology
Background:
- Angiogenesis is crucial for poststroke recovery.
- Understanding the molecular mechanisms of angiogenesis after stroke is vital.
- MicroRNAs play significant roles in regulating cellular processes, including angiogenesis.
Purpose of the Study:
- To investigate a microRNA-150 (miR-150)-based mechanism involved in cerebral angiogenesis after stroke.
- To explore the role of miR-150 in regulating vascular endothelial growth factor (VEGF) expression and function.
Main Methods:
- Established rat models of middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation cell models.
- Assessed angiogenesis markers including capillary density, tube formation, cell proliferation, and migration.
- Quantified miR-150 and VEGF expression using RT-PCR and Western blotting.
- Utilized dual-luciferase assays to confirm the interaction between miR-150 and VEGF.
Main Results:
- miR-150 expression was detected in brain and serum following cerebral ischemia and in oxygen-glucose-deprived brain microvascular endothelial cells (BMVECs) and astrocytes.
- Upregulated miR-150 reduced vascular density, tube formation, proliferation, and migration of BMVECs.
- miR-150 was confirmed to directly target and negatively regulate VEGF expression.
- VEGF mediated the effects of miR-150 on BMVEC functions.
Conclusions:
- miR-150 plays a regulatory role in cerebral poststroke angiogenesis in rats.
- The miR-150/VEGF axis is a key mechanism influencing angiogenesis after stroke.
- Targeting the miR-150 pathway may offer therapeutic potential for poststroke recovery.
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