ArticleThe Journal of biological chemistry2008
NFATc1 targets cyclin A in the regulation of vascular smooth muscle cell multiplication during restenosis.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
27 citing papers in PubMed, 37 citations in OpenAlex.
- The critical role of NFAT transcription factors in pulmonary arterial remodeling and pulmonary hypertension: from PASMC proliferation to therapeutic targeting.Molecular biology reports · 2026Review
- Diverse effects of calcineurin in vascular smooth muscle cells: physiological activators and the controversial actions of clinical inhibitors.Frontiers in pharmacology · 2026Review
- Cucurbitacins mitigate vascular neointimal hyperplasia by suppressing cyclin A2 expression and inhibiting VSMC proliferation.Animal models and experimental medicine · 2024Article
- NFAT activation by FKBP52 promotes cancer cell proliferation by suppressing p53.Life science alliance · 2024Article
- The Exacerbating Effects of the Tumor Necrosis Factor in Cardiovascular Stenosis: Intimal Hyperplasia.Cancers · 2024Review
- Hematopoietic Stem Cell Transcription Factors in Cardiovascular Pathology.Frontiers in genetics · 2020Review
- NFATc1-E2F1-LMCD1-Mediated IL-33 Expression by Thrombin Is Required for Injury-Induced Neointima Formation.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- LIM and cysteine-rich domains 1 is required for thrombin-induced smooth muscle cell proliferation and promotes atherogenesis.The Journal of biological chemistry · 2018Article
- CD137-CD137L interaction modulates neointima formation and the phenotype transformation of vascular smooth muscle cells via NFATc1 signaling.Molecular and cellular biochemistry · 2018Article
- Wnt signaling in cardiovascular disease: opportunities and challenges.Current opinion in lipidology · 2017Review
- Cell cycle and apoptosis regulation by NFAT transcription factors: new roles for an old player.Cell death & disease · 2016Review
- Vein graft failure.Journal of vascular surgery · 2015Review
- Cyclosporin A induces cardiac differentiation but inhibits hemato-endothelial differentiation of P19 cells.PloS one · 2015Article
- ERK activation is required for CCK-mediated pancreatic adaptive growth in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Store-operated CRAC channels regulate gene expression and proliferation in neural progenitor cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Effects of OX40-OX40L interaction on the nuclear factor of activated T cells c1 in ApoE-deficient mice.Inflammation · 2014Article
- Nuclear factor of activated T cells c1 mediates p21-activated kinase 1 activation in the modulation of chemokine-induced human aortic smooth muscle cell F-actin stress fiber formation, migration, and proliferation and injury-induced vascular wall remodeling.The Journal of biological chemistry · 2013Article
- OX40-OX40L interaction promotes proliferation and activation of lymphocytes via NFATc1 in ApoE-deficient mice.PloS one · 2013Article
- Protein kinase N1 is a novel substrate of NFATc1-mediated cyclin D1-CDK6 activity and modulates vascular smooth muscle cell division and migration leading to inward blood vessel wall remodeling.The Journal of biological chemistry · 2012Article
- Neonatal β cell development in mice and humans is regulated by calcineurin/NFAT.Developmental cell · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Platelet-derived growth factor BB (PDGF-BB) induced cyclin A expression and CDK2 activity in vascular smooth muscle cells (VSMC). Inhibition of nuclear factors of activated T cell (NFAT) activation by cyclosporin A (CsA) and VIVIT suppressed PDGF-BB-induced cyclin A expression and CDK2 activity, resulting in blockade of VSMC in the G(1) phase. In addition, CsA- and VIVIT-mediated inhibition of NFATs and small interfering RNA-targeted down-regulation of cyclin A levels suppressed PDGF-BB-induced VSMC DNA synthesis. PDGF-BB also induced cyclin A mRNA levels in VSMC in an NFAT-dependent manner. Cloning and bioinformatic analysis of rat cyclin A promoter revealed the presence of NFAT-binding elements, and PDGF-BB induced the binding of NFATs to these regulatory sequences in a CsA- and VIVIT-sensitive manner. Chromatin immunoprecipitation analysis showed that NFATc1 binds to the cyclin A promoter in response to PDGF-BB in a VIVIT-sensitive manner. Furthermore, PDGF-BB induced cyclin A promoter-luciferase reporter gene activity in VSMC, and it was inhibited by both CsA and VIVIT. Balloon injury induced cyclin A expression and CDK2 activity in rat carotid arteries, and these responses were also blocked by VIVIT. In addition, VIVIT attenuated balloon injury-induced SMC proliferation, resulting in reduced restenosis. Down-regulation of NFATc1 by its small interfering RNA inhibited PDGF-BB-induced cyclin A expression and DNA synthesis both in rat and human VSMC. Together, these findings demonstrate that the cyclin A-CDK2 complex may be a potential effector of NFATs, specifically NFATc1, in mediating SMC multiplication leading to neointima formation. Therefore, NFATs may be used as target molecules for the development of therapeutic agents against vascular diseases such as restenosis.
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Registered trials
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.