ArticleScientific reports2016
MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ).
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy.Reviews in endocrine & metabolic disorders · 2024Review
- Evaluation of Arterial Histopathology and microRNA Expression That Underlie Ultrasonography Findings in Temporal Arteries of Patients with Giant Cell Arteritis.International journal of molecular sciences · 2023Article
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- Expression of the microRNA-30 family in pulmonary arterial hypertension and the role of microRNA-30d-5p in the regulation of pulmonary arterial smooth muscle cell toxicity and apoptosis.Experimental and therapeutic medicine · 2022Article
- Current Status of MicroRNAs that Target the Wnt Signaling Pathway in Regulation of Osteogenesis and Bone Metabolism: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- miR-30b-5p Downregulation as a Predictive Biomarker of Coronary In-Stent Restenosis.Biomedicines · 2021Article
- Expression and Functional Analysis of lncRNAs Involved in Platelet-Derived Growth Factor-BB-Induced Proliferation of Human Aortic Smooth Muscle Cells.Frontiers in cardiovascular medicine · 2021Article
- MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy.Annals of translational medicine · 2020Article
- Exercise-associated prevention of adult cardiovascular disease in children and adolescents: monocytes, molecular mechanisms, and a call for discovery.Pediatric research · 2020Review
- Thymine DNA glycosylase is a key regulator of CaMKIIγ expression and vascular smooth muscle phenotype.American journal of physiology. Heart and circulatory physiology · 2019Article
- Elucidating the contributory role of microRNA to cardiovascular diseases (a review).Vascular pharmacology · 2019Review
- Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing.Oxidative medicine and cellular longevity · 2018Review
- MicroRNA-30e-5p promotes cell growth by targeting PTPN13 and indicates poor survival and recurrence in lung adenocarcinoma.Journal of cellular and molecular medicine · 2017Article
- Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation.Oncotarget · 2017Article
- The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis.Tzu chi medical journalReview
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The multifunctional Ca(2+)/calmodulin-dependent protein kinase II δ-isoform (CaMKIIδ) promotes vascular smooth muscle (VSM) proliferation, migration, and injury-induced vascular wall neointima formation. The objective of this study was to test if microRNA-30 (miR-30) family members are endogenous regulators of CaMKIIδ expression following vascular injury and whether ectopic expression of miR-30 can inhibit CaMKIIδ-dependent VSM cell function and neointimal VSM hyperplasia induced by vascular injury. The CaMKIIδ 3'UTR contains a consensus miR-30 binding sequence that is highly conserved across species. A significant decrease in miR-30 family members and increase in CaMKIIδ2 protein expression, with no change in CaMKIIδ mRNA expression, was observed in medial layers of VSM 7 days post-injury. In vitro, overexpression of miR-30c or miR-30e inhibited CaMKIIδ2 protein expression by ~50% in cultured rat aortic VSM cells, and inhibited VSM cell proliferation and migration. In vivo, lenti-viral delivery of miR-30c into injured rat carotid arteries prevented the injury-induced increase in CaMKIIδ2. Furthermore, neointima formation was dramatically inhibited by lenti-viral delivery of miR-30c in the injured medial smooth muscle. These studies define a novel mechanism for regulating CaMKIIδ expression in VSM and provide a new potential therapeutic strategy to reduce progression of vascular proliferative diseases, including atherosclerosis and restenosis.
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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.