ArticleArteriosclerosis, thrombosis, and vascular biology2013
MicroRNA-145 restores contractile vascular smooth muscle phenotype and coronary collateral growth in the metabolic syndrome.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- MicroRNA-125b in vascular diseases: An updated systematic review of pathogenetic implications and clinical applications.Journal of cellular and molecular medicine · 2019Pooled it
- S-nitrosylation of AMPKγ impairs coronary collateral circulation and disrupts VSMC reprogramming.EMBO reports · 2024Article
- Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer.International journal of molecular sciences · 2023Article
- 20-Hydroxyeicosatetraenoic acid (20-HETE): Bioactions, receptors, vascular function, cardiometabolic disease and beyond.Advances in pharmacology (San Diego, Calif.) · 2023Article
- MicroRNAs in T Cell-Immunotherapy.International journal of molecular sciences · 2022Review
- MicroRNAs as therapeutic targets in breast cancer metastasis.Drug delivery and translational research · 2022Review
- Knock-out of MicroRNA 145 impairs cardiac fibroblast function and wound healing post-myocardial infarction.Journal of cellular and molecular medicine · 2020Article
- miR-145 inhibits the proliferation and migration of vascular smooth muscle cells by regulating autophagy.Journal of cellular and molecular medicine · 2020Article
- MiR-145 alleviates Hcy-induced VSMC proliferation, migration, and phenotypic switch through repression of the PI3K/Akt/mTOR pathway.Histochemistry and cell biology · 2020Article
- MicroRNA-145 targets in cancer and the cardiovascular system: evidence for common signaling pathways.Vascular biology (Bristol, England) · 2020Review
- Circulating miRNA-23b and miRNA-143 Are Potential Biomarkers for In-Stent Restenosis.BioMed research international · 2020Article
- Core-Shell Polymer-Based Nanoparticles Deliver miR-155-5p to Endothelial Cells.Molecular therapy. Nucleic acids · 2019Article
- Dysregulation of Epigenetic Mechanisms of Gene Expression in the Pathologies of Hyperhomocysteinemia.International journal of molecular sciences · 2019Review
- Comparison of Cardiovascular Benefits of Bariatric Surgery and Abdominal Lipectomy.Current hypertension reports · 2019Review
- Cholesterol induces dedifferentiation of vascular smooth muscle cells by regulating monocyte chemotactic protein-1-induced protein 1.International journal of clinical and experimental pathology · 2019Article
- Hypermethylation of the Micro-RNA 145 Promoter Is the Key Regulator for NLRP3 Inflammasome-Induced Activation and Plaque Formation.JACC. Basic to translational science · 2018Article
- Elevated 20-HETE in metabolic syndrome regulates arterial stiffness and systolic hypertension via MMP12 activation.Journal of molecular and cellular cardiology · 2018Article
- The protective effect of cardamonin on the factors involved in delayed cerebral vasospasm in a rat model of subarachnoid hemorrhage.International journal of clinical and experimental pathology · 2018Article
- Plasma Omentin-1 Level as a Predictor of Good Coronary Collateral Circulation.Journal of atherosclerosis and thrombosis · 2017Article
- Improving miRNA Delivery by Optimizing miRNA Expression Cassettes in Diverse Virus Vectors.Human gene therapy methods · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTransient, repetitive occlusion stimulates coronary collateral growth (CCG) in normal animals. Vascular smooth muscle cells (VSMCs) switch to synthetic phenotype early in CCG, then return to contractile phenotype. CCG is impaired in the metabolic syndrome. We determined whether impaired CCG was attributable to aberrant VSMC phenotypic modulation by miR-145-mediated mechanisms, and whether restoration of physiological miR-145 levels in metabolic syndrome (JCR rat) improved CCG. APPROACH AND
resultsCCG was stimulated by transient, repetitive left anterior descending artery occlusion and evaluated after 9 days by coronary blood flow measurements (microspheres). miR-145 was delivered to JCR VSMCs via adenoviral vector (miR-145-Adv). In JCR rats, miR-145 was decreased late in CCG (≈ 2-fold day 6; ≈ 4-fold day 9 versus SD), which correlated with decreased expression of smooth muscle-specific contractile proteins (≈ 5-fold day 6; ≈ 10-fold day 9 versus SD), indicative of VSMCs' failure to return to the contractile phenotype late in CCG. miR-145 expression in JCR rats (miR-145-Adv) on days 6 to 9 of CCG completely restored VSMCs contractile phenotype and CCG (collateral/normal zone flow ratio was 0.93 ± 0.09 JCR+miR-145-Adv versus 0.12 ± 0.02 JCR versus 0.87 ± 0.02 SD).
conclusionsRestoration of VSMC contractile phenotype through miR-145 delivery is a highly promising intervention for restoration of CCG in the metabolic syndrome.
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