ArticleCNS neuroscience & therapeutics2016
MiR-150 Regulates Poststroke Cerebral Angiogenesis via Vascular Endothelial Growth Factor in Rats.
Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- Prenatal alcohol exposure-mediated Tet1 upregulation promotes DNA demethylation and elevated transcription at the miR-150 promoter.American journal of physiology. Cell physiology · 2026Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- Transcription Factor TFAP2B Exerts Neuroprotective Effects Targeting BNIP3-Mediated Mitophagy in Ischemia/Reperfusion Injury.Molecular neurobiology · 2024Article
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- Diverse activity of miR-150 in Tumor development: shedding light on the potential mechanisms.Cancer cell international · 2023Review
- MicroRNA Expression Profile in Bone Marrow and Lymph Nodes in B-Cell Lymphomas.International journal of molecular sciences · 2023Article
- Angiogenesis after ischemic stroke.Acta pharmacologica Sinica · 2023Review
- The various role of microRNAs in breast cancer angiogenesis, with a special focus on novel miRNA-based delivery strategies.Cancer cell international · 2023Review
- MicroRNA-150-5p is upregulated in the brain microvasculature during prenatal alcohol exposure and inhibits the angiogenic factor Vezf1.Alcoholism, clinical and experimental research · 2022Article
- Exosomal microRNA-150-5p from bone marrow mesenchymal stromal cells mitigates cerebral ischemia/reperfusion injury via targeting toll-like receptor 5.Bioengineered · 2022Article
- Amphibian-derived peptide homodimer OA-GL17d promotes skin wound regeneration through the miR-663a/TGF-β1/Smad axis.Burns & trauma · 2022Article
- Article
- Not All Lectins Are Equally Suitable for Labeling Rodent Vasculature.International journal of molecular sciences · 2021Article
- Foxo1-induced miR-92b down-regulation promotes blood-brain barrier damage after ischaemic stroke by targeting NOX4.Journal of cellular and molecular medicine · 2021Article
- Long Non-coding RNAs as Promising Therapeutic Approach in Ischemic Stroke: a Comprehensive Review.Molecular neurobiology · 2021Review
- A Feedback Loop Involving MicroRNA-150 and MYB Regulates VEGF Expression in Brain Microvascular Endothelial Cells After Oxygen Glucose Deprivation.Frontiers in physiology · 2021Article
- EGb761 Protects Brain Microvascular Endothelial Cells Against Oxygen-Glucose Deprivation-Induced Injury Through lncRNA Rmst/miR-150 Axis.Neurochemical research · 2020Article
- Decreased miR-150 in obesity-associated type 2 diabetic mice increases intraocular inflammation and exacerbates retinal dysfunction.BMJ open diabetes research & care · 2020Article
- Endothelium-Targeted Deletion of microRNA-15a/16-1 Promotes Poststroke Angiogenesis and Improves Long-Term Neurological Recovery.Circulation research · 2020Article
- MicroRNAs and Regeneration in Animal Models of CNS Disorders.Neurochemical research · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAngiogenesis 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.
methodsRat 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.
resultsWe 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.
conclusionsOur data suggested that miR-150 could regulate cerebral poststroke angiogenesis in rats through VEGF.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.