ArticleThe Journal of biological chemistry2013
CaMKIIδ-dependent inhibition of cAMP-response element-binding protein activity in vascular smooth muscle.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed.
- Potential therapeutic mechanisms ofFrontiers in pharmacology · 2025Review
- Inositol 1,4,5-Trisphosphate Receptors Regulate Vascular Smooth Muscle Cell Proliferation and Neointima Formation in Mice.Journal of the American Heart Association · 2024Article
- Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy.Reviews in endocrine & metabolic disorders · 2024Review
- Multi-faceted regulation of CREB family transcription factors.Frontiers in molecular neuroscience · 2024Review
- Calcium Signalling in Heart and Vessels: Role of Calmodulin and Downstream Calmodulin-Dependent Protein Kinases.International journal of molecular sciences · 2022Review
- Article
- What turns CREB on? And off? And why does it matter?Cellular and molecular life sciences : CMLS · 2020Review
- The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis.International journal of molecular sciences · 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
- CAMKII as a therapeutic target for growth factor-induced retinal and choroidal neovascularization.JCI insight · 2019Article
- CaMKII (CaArteriosclerosis, thrombosis, and vascular biology · 2018Article
- Nampt/RelB pathway protects learning and memory ability in aged rats after general anesthesia with sevoflurane and nitrous oxide.International journal of clinical and experimental pathology · 2018Article
- Role of CaMKII in Ang-II-dependent small artery remodeling.Vascular pharmacology · 2016Article
- Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016Review
- MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ).Scientific reports · 2016Article
- Ca2+/calmodulin-dependent protein kinase II-γ (CaMKIIγ) negatively regulates vascular smooth muscle cell proliferation and vascular remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.Journal of the American Heart Association · 2015Article
- 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
5 authors.
Funding
Abstract
One transcription factor mediator of Ca(2+)-signals is cAMP response element-binding protein (CREB). CREB expression and/or activity negatively correlates with vascular smooth muscle (VSM) cell proliferation and migration. Multifunctional Ca(2+)/calmodulin-dependent protein kinases, including CaMKII, have been demonstrated to regulate CREB activity through both positive and negative phosphorylation events in vitro, but the function of CaMKII as a proximal regulator of CREB in intact cell systems, including VSM, is not clear. In this study, we used gain- and loss-of-function approaches to determine the function of CaMKIIδ in regulating CREB phosphorylation, localization, and activity in VSM. Overexpression of constitutively active CaMKIIδ specifically increased CREB phosphorylation on Ser(142) and silencing CaMKIIδ expression by siRNA or blocking endogenous CaMKII activity with KN93 abolished thrombin- or ionomycin-induced CREB phosphorylation on Ser(142) without affecting Ser(133) phosphorylation. CREB-Ser(142) phosphorylation correlated with transient nucleocytoplasmic translocation of CREB. Thrombin-induced CREB promoter activity, CREB binding to Sik1 and Rgs2 promoters, and Sik1/Rgs2 transcription were enhanced by a kinase-negative CaMKIIδ2 (K43A) mutant and inhibited by a constitutively active (T287D) mutant. Taken together, these studies establish negative regulation of CREB activity by endogenous CaMKIIδ-dependent CREB-Ser(142) phosphorylation and suggest a potential mechanism for CaMKIIδ/CREB signaling in modulating proliferation and migration in VSM cells.
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