ArticleActa pharmacologica Sinica2009
Calcineurin-NFAT signaling is involved in phenylephrine-induced vascular smooth muscle cell proliferation.
Article in Acta pharmacologica Sinica, 2009. 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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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Leiomodin 1 deficiency promotes lipid accumulation and redirects gene regulatory programs in smooth muscle cells exposed to oxidized LDL.Research square · 2026Article
- Sex-Dependent Effects of Angiotensin II and Calcineurin in the Vasculature of Mice.Acta physiologica (Oxford, England) · 2026Article
- Artery tertiary lymphoid organs, neuro-immune interaction and their mediators in atherosclerosis.Basic research in cardiology · 2026Review
- Preventive and inhibitory effects ofBiochemistry and biophysics reports · 2026Article
- Diverse effects of calcineurin in vascular smooth muscle cells: physiological activators and the controversial actions of clinical inhibitors.Frontiers in pharmacology · 2026Review
- Inositol 1,4,5-Trisphosphate Receptors Regulate Vascular Smooth Muscle Cell Proliferation and Neointima Formation in Mice.Journal of the American Heart Association · 2024Article
- Vascular dysfunction caused by loss of Brn-3b/POU4F2 transcription factor in aortic vascular smooth muscle cells is linked to deregulation of calcium signalling pathways.Cell death & disease · 2023Article
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Vascular Health Triad in Humans With Hypertension-Not the Usual Suspects.Frontiers in physiology · 2021Review
- Role of NFAT in the Progression of Diabetic Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- p62/sequestosome 1 deficiency accelerates osteoclastogenesisThe Journal of biological chemistry · 2018Article
- Gene expression profiles and signaling mechanisms in αBMC systems biology · 2017Article
- Calcineurin/NFAT Activation-Dependence of Leptin Synthesis and Vascular Growth in Response to Mechanical Stretch.Frontiers in physiology · 2016Article
- Nuclear factor of activated T-cell isoform expression and regulation in human myometrium.Reproductive biology and endocrinology : RB&E · 2015Article
- CD137 Regulates NFATc1 Expression in Mouse VSMCs through TRAF6/NF-κB p65 Signaling Pathway.Mediators of inflammation · 2015Article
- Calcineurin mediates synaptic scaling via synaptic trafficking of Ca2+-permeable AMPA receptors.PLoS biology · 2014Article
- Cypher/ZASP is a novel A-kinase anchoring protein.The Journal of biological chemistry · 2013Article
- Therapeutic potential for protein kinase C inhibitor in vascular restenosis.Journal of cardiovascular pharmacology and therapeutics · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimCatecholamine-induced vascular smooth muscle cell (VSMC) proliferation is one of the major events in the pathogenesis of atherosclerosis and vascular remodeling. The calcineurin-NFAT pathway plays a role in regulating growth and differentiation in various cell types. We investigated whether the calcineurin-NFAT pathway was involved in the regulation of phenylephrine-induced VSMC proliferation.
methodsProliferation of VSMC was measured using an MTT assay and cell counts. Localization of NFATc1 was detected by immunofluorescence staining. NFATc1-DNA binding was determined by EMSA and luciferase activity analyses. NFATc1 and calcineurin levels were assayed by immunoprecipitation.
resultsPhenylephrine (PE, an alpha(1)-adrenoceptor agonist) increased VSMC proliferation and cell number. Prazosin (an alpha(1)-adrenoceptor antagonist), cyclosporin A (CsA, an inhibitor of calcineurin) and chelerythrine (an inhibitor of PKC) decreased PE-induced proliferation and cell number. Additional treatment of VSMC with CsA or chelerythrine further inhibited proliferation and cell number in the chelerythrine-pretreatment group and the CsA-pretreatment group. CsA and chelerythrine alone had no effect on either absorbance or cell number. CsA decreased PE-induced calcineurin levels and activity. NFATc1 was translocated from the cytoplasm to the nucleus upon treatment with PE. This translocation was reversed by CsA. CsA decreased the PE-induced NFATc1 level in the nucleus. PE increased NFAT's DNA binding activity and NFAT-dependent reporter gene expression. CsA blocked these effects.
conclusionCsA partially suppresses PE-induced VSMC proliferation by inhibiting calcineurin activity and NFATc1 nuclear translocation. The calcineurin-NFATc1 pathway is involved in the hyperplastic growth of VSMC induced by phenylephrine.
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