ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016
Ca2+/calmodulin-dependent protein kinase II-γ (CaMKIIγ) negatively regulates vascular smooth muscle cell proliferation and vascular remodeling.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy.Reviews in endocrine & metabolic disorders · 2024Review
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- Calcium/calmodulin-dependent protein kinase IV regulates vascular autophagy and insulin signaling through Akt/mTOR/CREB pathway in ob/ob mice.Journal of physiology and biochemistry · 2022Article
- Pharmacological analysis of Empagliflozin: Acting through the CaMKII pathway in type 2 diabetes and acute cardiovascular events.PloS one · 2022Article
- Combination of Genomic and Transcriptomic Approaches Highlights Vascular and Circadian Clock Components in Multiple Sclerosis.International journal of molecular sciences · 2021Article
- Article
- CaMKIIδ is upregulated by pro-inflammatory cytokine IL-6 in a JAK/STAT3-dependent manner to promote angiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Resveratrol Inhibits Neointimal Growth after Arterial Injury in High-Fat-Fed Rodents: The Roles of SIRT1 and AMPK.Journal of vascular research · 2020Article
- Thymine DNA glycosylase is a key regulator of CaMKIIγ expression and vascular smooth muscle phenotype.American journal of physiology. Heart and circulatory physiology · 2019Article
- CaMKII Activity in the Inflammatory Response of Cardiac Diseases.International journal of molecular sciences · 2019Review
- Overexpression ofOncology letters · 2018Article
- CRISPR-Cas9-Mediated Epitope Tagging Provides Accurate and Versatile Assessment of Myocardin-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Endothelial Myocyte Enhancer Factor 2c Inhibits Migration of Smooth Muscle Cells Through Fenestrations in the Internal Elastic Lamina.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Role of CaMKII in Ang-II-dependent small artery remodeling.Vascular pharmacology · 2016Article
- MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ).Scientific reports · 2016Article
- Differentiation of Human Adipose Derived Stem Cells into Smooth Muscle Cells Is Modulated by CaMKIIγ.Stem cells international · 2016Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Vascular smooth muscle (VSM) expresses calcium/calmodulin-dependent protein kinase II (CaMKII)-δ and -γ isoforms. CaMKIIδ promotes VSM proliferation and vascular remodeling. We tested CaMKIIγ function in vascular remodeling after injury. CaMKIIγ protein decreased 90% 14 d after balloon injury in rat carotid artery. Intraluminal transduction of adenovirus encoding CaMKIIγC rescued expression to 35% of uninjured controls, inhibited neointima formation (>70%), inhibited VSM proliferation (>60%), and increased expression of the cell-cycle inhibitor p21 (>2-fold). Comparable doses of CaMKIIδ2 adenovirus had no effect. Similar dynamics in CaMKIIγ mRNA and protein expression were observed in ligated mouse carotid arteries, correlating closely with expression of VSM differentiation markers. Targeted deletion of CaMKIIγ in smooth muscle resulted in a 20-fold increase in neointimal area, with a 3-fold increase in the cell proliferation index, no change in apoptosis, and a 60% decrease in p21 expression. In cultured VSM, CaMKIIγ overexpression induced p53 mRNA (1.7 fold) and protein (1.8-fold) expression; induced the p53 target gene p21 (3-fold); decreased VSM cell proliferation (>50%); and had no effect on expression of apoptosis markers. We conclude that regulated CaMKII isoform composition is an important determinant of the injury-induced vasculoproliferative response and that CaMKIIγ and -δ isoforms have nonequivalent, opposing functions.
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Registered trials
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