ArticleScientific reports2017
Secreted miR-27a Induced by Cyclic Stretch Modulates the Proliferation of Endothelial Cells in Hypertension via GRK6.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Mechanotransduction through oxidative stress upregulates circLyst to drive vascular remodeling in hypertensive humans and rodents.Molecular biomedicine · 2026Article
- Oxidative stress-induced endothelial dysfunction drives mechanical and infectious lung injury: Therapeutic potential of kaempferol in males.Redox biology · 2026Article
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- A Bibliometric Analysis of P2X7R in Cardiovascular Diseases from 2005 to 2024.Current cardiology reviews · 2026Review
- Pathogenic and clinical significance of inflammation-associated MicroRNAs in cardiovascular diseases.Molecular biology reports · 2025Review
- CircRNA-based AntimiR therapy: A novel approach to hypertension treatment.Non-coding RNA research · 2025Review
- Diversity of extracellular vesicle sources in atherosclerosis: role and therapeutic application.Angiogenesis · 2025Review
- Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1.Mechanobiology in medicine · 2025Article
- Injury and cyclic stretch induce vein graft failure: effective treatment with zinc oxide-loaded electrospun polycaprolactone external stent.Regenerative biomaterials · 2025Article
- G protein-coupled receptor kinases in hypertension: physiology, pathogenesis, and therapeutic targets.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Platelet-derived microvesicles drive vascular smooth muscle cell migration via forming podosomes and promoting matrix metalloproteinase-9 activity.Mechanobiology in medicine · 2023Article
- Systems Biology Analysis of Temporal Dynamics That Govern Endothelial Response to Cyclic Stretch.Biomolecules · 2022Review
- Comprehensive insights in GRK4 and hypertension: From mechanisms to potential therapeutics.Pharmacology & therapeutics · 2022Review
- Platelet membrane-camouflaged nanoparticles carry microRNA inhibitor against myocardial ischaemia‒reperfusion injury.Journal of nanobiotechnology · 2022Article
- Differential and targeted vesiculation: pathologic cellular responses to elevated arterial pressure.Molecular and cellular biochemistry · 2022Review
- FRET Visualization of Cyclic Stretch-Activated ERKFrontiers in cell and developmental biology · 2022Article
- Single-cell analysis of salt-induced hypertensive mouse aortae reveals cellular heterogeneity and state changes.Experimental & molecular medicine · 2021Article
- Regulation of microRNA-221, -222, -21 and -27 in articular cartilage subjected to abnormal compressive forces.The Journal of physiology · 2021Article
- Extracellular vesicles: Potential impact on cardiovascular diseases.Advances in clinical chemistry · 2021Review
- In Vitro/Ex Vivo Models for the Study of Ischemia Reperfusion Injury during Kidney Perfusion.International journal of molecular sciences · 2020Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal proliferation of endothelial cells (ECs) is important in vascular remodeling during hypertension, but the mechanisms are still unclear. In hypertensive rats caused by abdominal aortic coarctation, the expression of G-protein-coupled receptor kinase 6 (GRK6) in ECs at common carotid artery was repressed in vivo, and EC proliferation was increased. 15% cyclic stretch in vitro, which mimics the pathologically increased stretch in hypertension, repressed EC GRK6 expression via paracrine control by vascular smooth muscle cells (VSMCs). Furthermore, VSMC-derived microparticles (VSMC-MPs) were detected in the conditioned medium from VSMCs and in artery. VSMC-MPs from cells exposed to 15% cyclic stretch decreased GRK6 expression and increased EC proliferation. miR-27a was detected in VSMC-MPs and was upregulated by 15% cyclic stretch. miR-27a was transferred from VSMCs to ECs via VSMC-MPs and directly targeted on GRK6. Finally, a multi-point injection of antagomiR-27a around carotid artery decreased miR-27a expression in vivo, induced GRK6 expression, and reversed the abnormal EC proliferation. Pathologically elevated cyclic stretch increased the secretion of miR-27a, which was transferred from VSMCs to ECs via the VSMC-MPs, subsequently targeted GRK6, and induced EC proliferation. Locally decreasing miR-27a could be a novel therapeutic approach to attenuate the abnormal EC proliferation in hypertension.
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