ArticleScientific reports2017
MicroRNA-26a targets MAPK6 to inhibit smooth muscle cell proliferation and vein graft neointimal hyperplasia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- AAV2.7m8-Mediated MicroRNA Expression Suppresses VEGF-Induced Angiogenic Responses in HUVEC.International journal of molecular sciences · 2026Article
- Effects of MicroRNA-19b Carried by Endothelial Microparticles on the Phenotypic Switching of Vascular Smooth Muscle Cells and the Working Mechanism.Bulletin of experimental biology and medicine · 2025Article
- Anticancer Effects of MAPK6 siRNA-Loaded PLGA Nanoparticles in the Treatment of Breast Cancer.Journal of cellular and molecular medicine · 2025Article
- Identification of metabolic biomarkers in idiopathic pulmonary arterial hypertension using targeted metabolomics and bioinformatics analysis.Scientific reports · 2024Article
- Unraveling the miRNA Puzzle in Atherosclerosis: Revolutionizing Diagnosis, Prognosis, and Therapeutic Approaches.Current atherosclerosis reports · 2024Review
- ERK3 is involved in regulating cardiac fibroblast function.Physiological reports · 2024Article
- Mapping cardiac remodeling in chronic kidney disease.Science advances · 2023Article
- MiR-3571 modulates the proliferation and migration of vascular smooth muscle cells by targeting claudin 1.International journal of medical sciences · 2022Article
- Identification of Crucial Hub Genes and Differential T Cell Infiltration in Idiopathic Pulmonary Arterial Hypertension Using Bioinformatics Strategies.Frontiers in molecular biosciences · 2022Article
- MAPK6-AKT signaling promotes tumor growth and resistance to mTOR kinase blockade.Science advances · 2021Article
- A microRNA‑17‑5p/homeobox B13 axis participates in the phenotypic modulation of vascular smooth muscle cells.Molecular medicine reports · 2021Article
- MicroRNA‑524‑5p regulates the proliferation and invasion of HTR‑8/SVneo trophoblasts by targeting NUMB in the Notch signaling pathway.Molecular medicine reports · 2021Article
- LncRNA GAS6-AS2 promotes non-small-cell lung cancer cell proliferation via regulating miR-144-3p/ MAPK6 axis.Cell cycle (Georgetown, Tex.) · 2021Article
- A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application.Journal of visualized experiments : JoVE · 2020Article
- Article
- LncRNA SNHG1 regulates vascular endothelial cell proliferation and angiogenesis via miR-196a.Journal of molecular histology · 2020Article
- An Aligned Patterned Biomimetic Elastic Membrane Has a Potential as Vascular Tissue Engineering Material.Frontiers in bioengineering and biotechnology · 2020Article
- Interfering histone deacetylase 4 inhibits the proliferation of vascular smooth muscle cells via regulating MEG3/miR-125a-5p/IRF1.Cell adhesion & migration · 2019Article
- The atypical MAPK ERK3 potently suppresses melanoma cell growth and invasiveness.Journal of cellular physiology · 2019Article
- MiR-9 promotes the phenotypic switch of vascular smooth muscle cells by targeting KLF5Turkish journal of medical sciences · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neointima formation is the major reason for vein graft failure. However, the underlying mechanism is unclear. The aim of this study was to determine the role of miR-26a in the development of neointimal hyperplasia of autogenous vein grafts. Using autologous jugular vein grafts in the rat carotid artery as a model, we found that miR-26a was significantly downregulated in grafted veins as well as proliferating vascular smooth muscle cells (VSMCs) stimulated with platelet-derived growth factor-BB (PDGF-BB). Overexpression of miR-26a reduced the proliferation and migration of VSMCs. Further analysis revealed that the effects of miR-26a in VSMCs were mediated by targeting MAPK6 at the mRNA and protein levels. Luciferase assays showed that miR-26a repressed wild type (WT) MAPK6-3'-UTR-luciferase activity but not mutant MAPK6-3'-UTR-luciferease reporter. MAPK6 deficiency reduced proliferation and migration; in contrast, overexpression of MAPK6 enhanced the proliferation and migration of VSMCs. This study confirmed that neointimal hyperplasia in vein grafts was reduced in vivo by up-regulated miR-26a expression. In conclusion, our results showed that miR-26a is an important regulator of VSMC functions and neointimal hyperplasia, suggesting that miR-26a may be a potential therapeutic target for autologous vein graft diseases.
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