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Updated: Feb 13, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
MiR-103 regulates the angiogenesis of ischemic stroke rats by targeting vascular endothelial growth factor (VEGF)
Fu-Ping Shi1, Xue-Hong Wang2, Hong-Xin Zhang3
1Department of Neurology, Affiliated Hospital of Hebei University, Baoding 071000, Hebei Province, China.
Objectives:
To investigate the effect of miR-103 on the angiogenesis of ischemic stroke rats via targeting vascular endothelial growth factor (VEGF) at the molecular level.
Materials And Methods:
Rat models had received the middle cerebral artery occlusion (MCAO) or sham operation before grouping, and cell models of oxygen-glucose deprivation (OGD) were performed. FITC-dextran, matrigel, and Trans-well assays were used to evaluate the vascular density, tube formation, and cell migration respectively. The expression levels of miR-103 and VEGF were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Dual-luciferase assay was used for analyzing the targeting relationship between miR-103 and VEGF.
Results:
We found the reduced miR-103 in rats after MCAO. Down-regulating miR-103 with the miR-103 inhibitor enhanced VEGF, ameliorated the neurological scores, decreased infarct volume, and increased vascular density in rats after MCAO. Besides, in OGD human umbilical vein endothelial cells (HUVECs), inhibition of miR-103 could promote the increase of tube length and the migration of cells. Additionally, we found that miR-103 could directly target VEGF and thereby lead to the down-expression of VEGF. Meanwhile, si-VEGF could reverse the effect of miR-103 inhibitor on angiogenesis in rats subjected to MCAO.
Conclusion:
Inhibition of miR-103 could promote ischemic stroke angiogenesis and reduce infarction volume via enhancing VEGF, which provides a new target for the clinical treatment of ischemic stroke.
Insights
Inhibiting microRNA-103 (miR-103) promotes blood vessel formation in ischemic stroke by increasing vascular endothelial growth factor (VEGF). This finding offers a new therapeutic target for reducing stroke damage.
Area of Science:
- Molecular Biology
- Neuroscience
- Cardiovascular Biology
Background:
- Ischemic stroke is a leading cause of disability worldwide.
- Angiogenesis plays a critical role in recovery after ischemic stroke.
- MicroRNAs (miRNAs) are implicated in various cellular processes, including angiogenesis.
Purpose of the Study:
- To investigate the role of miR-103 in the angiogenesis of ischemic stroke.
- To determine if miR-103 targets vascular endothelial growth factor (VEGF).
- To explore the therapeutic potential of modulating miR-103 in ischemic stroke.
Main Methods:
- Rat models of middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation (OGD) cell models were used.
- Vascular density, tube formation, and cell migration were assessed.
- Quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and dual-luciferase assays were employed to analyze miR-103 and VEGF expression and their interaction.
Main Results:
- miR-103 expression was reduced in MCAO rats.
- Inhibition of miR-103 increased VEGF expression, improved neurological scores, reduced infarct volume, and enhanced vascular density.
- miR-103 directly targets VEGF, leading to its downregulation.
- Silencing VEGF reversed the pro-angiogenic effects of miR-103 inhibition.
Conclusions:
- Inhibition of miR-103 promotes angiogenesis and reduces infarction volume in ischemic stroke by enhancing VEGF.
- Modulating miR-103 represents a potential therapeutic strategy for ischemic stroke treatment.
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