ArticleArteriosclerosis, thrombosis, and vascular biology2011
Nuclear factor of activated T cells 5 regulates vascular smooth muscle cell phenotypic modulation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Gene-centric meta-analysis in 87,736 individuals of European ancestry identifies multiple blood-pressure-related loci.American journal of human genetics · 2014Pooled it
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- NCOR1 maintains the homeostasis of vascular smooth muscle cells and protects against aortic aneurysm.Cell death and differentiation · 2023Article
- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
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- High NaBiomedicines · 2021Review
- Single-Cell Epigenomics and Functional Fine-Mapping of Atherosclerosis GWAS Loci.Circulation research · 2021Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- MiR-223/NFAT5 signaling suppresses arterial smooth muscle cell proliferation and motilityAging · 2020Article
- Co-expression of glycosylated aquaporin-1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis-prone mice.Journal of cellular and molecular medicine · 2020Article
- Circulating miR-206 and Wnt-signaling are associated with cardiovascular complications and a history of preeclampsia in women.Clinical science (London, England : 1979) · 2020Article
- Drug-Eluting Stent Targeting Sp-1-Attenuated Restenosis by Engaging YAP-Mediated Vascular Smooth Muscle Cell Phenotypic Modulation.Journal of the American Heart Association · 2020Article
- Potential Role of Gene Regulator NFAT5 in the Pathogenesis of Diabetes Mellitus.Journal of diabetes research · 2020Review
- Impaired smooth muscle cell contractility as a novel concept of abdominal aortic aneurysm pathophysiology.Scientific reports · 2019Article
- Role of NFAT5 in the Immune System and Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2019Review
- NFAT5 Isoform C Controls Biomechanical Stress Responses of Vascular Smooth Muscle Cells.Frontiers in physiology · 2018Article
- Biomechanical Stretch Induces Inflammation, Proliferation, and Migration by Activating NFAT5 in Arterial Smooth Muscle Cells.Inflammation · 2017Article
- Understanding the Two Faces of Low-Salt Intake.Current hypertension reports · 2017Review
- Expression, fermentation and purification of a predicted intrinsically disordered region of the transcription factor, NFAT5.Protein expression and purification · 2015Article
- PKC-α contributes to high NaCl-induced activation of NFAT5 (TonEBP/OREBP) through MAPK ERK1/2.American journal of physiology. Renal physiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe tonicity-responsive transcription factor, nuclear factor of activated T cells 5 (NFAT5/tonicity enhancer binding protein [TonEBP]), has been well characterized in numerous cell types; however, NFAT5 function in vascular smooth muscle cells (SMCs) is unknown. Our main objective was to determine the role of NFAT5 regulation in SMCs. METHODS AND
resultsWe showed that NFAT5 is regulated by hypertonicity in SMCs and is upregulated in atherosclerosis and neointimal hyperplasia. RNAi knockdown of NFAT5 inhibited basal expression of several SMC differentiation marker genes, including smooth muscle α actin (SMαA). Bioinformatic analysis of SMαA revealed 7 putative NFAT5 binding sites in the first intron, and chromatin immunoprecipitation analysis showed NFAT5 enrichment of intronic DNA. Overexpression of NFAT5 increased SMαA promoter-intron activity, which requires an NFAT5 cis element at +1012, whereas dominant-negative NFAT5 decreased SMαA promoter-intron activity. Because it is unlikely that SMCs experience extreme changes in tonicity, we investigated other stimuli and uncovered 2 novel NFAT5-inducing factors: angiotensin II, a contractile agonist, and platelet-derived growth factor-BB (PDGF-BB), a potent mitogen in vascular injury. Angiotensin II stimulated NFAT5 translocation and activity, and NFAT5 knockdown inhibited an angiotensin II-mediated upregulation of SMαA mRNA. PDGF-BB increased NFAT5 protein, and loss of NFAT5 inhibited PDGF-BB-induced SMC migration.
conclusionsWe have identified NFAT5 as a novel regulator of SMC phenotypic modulation and have uncovered the role of NFAT5 in angiotensin II-induced SMαA expression and PDGF-BB-stimulated SMC migration.
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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.