ArticleArteriosclerosis, thrombosis, and vascular biology2019
NFATc1-E2F1-LMCD1-Mediated IL-33 Expression by Thrombin Is Required for Injury-Induced Neointima Formation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 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
- IL-33 blockade attenuates vascular inflammation in a mouse model of Kawasaki disease vasculitis.Clinical and experimental immunology · 2026Article
- Evaluation of radiogenomics for risk stratification of intracranial aneurysms: a pilot study.Neuroradiology · 2025Article
- Evaluation of Radiogenomics for Risk Stratification of Intracranial Aneurysms: A Pilot Study.Research square · 2025Article
- Innovative Atherosclerosis Models: Advancing Pathophysiology and Translational Research.Research (Washington, D.C.) · 2025Review
- Transcriptome analysis of 3D4/21 cells expressing CSFV NS4B.Frontiers in microbiology · 2025Article
- IL-33/ST2 axis mediates diesel exhaust particles-induced mast cell activation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Early Injury Landscape in Vein Harvest by Single-Cell and Spatial Transcriptomics.Circulation research · 2024Article
- Integrated single-nuclei and spatial transcriptomic analysis reveals propagation of early acute vein harvest and distension injury signaling pathways following arterial implantation.bioRxiv : the preprint server for biology · 2024Article
- Differences in vascular endothelial function and serum proteome between obese people with phlegm-dampness constitution and balanced constitution.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Integrative analysis of HASMCs gene expression profile revealed the role of thrombin in the pathogenesis of atherosclerosis.BMC cardiovascular disorders · 2023Article
- Blockade of CD47 function attenuates restenosis by promoting smooth muscle cell efferocytosis and inhibiting their migration and proliferation.The Journal of biological chemistry · 2023Article
- Identification of candidate biomarkers and mechanisms in foam cell formation from heterogeneous cellular origins via integrated transcriptome analysis.Annals of translational medicine · 2023Article
- Article
- The Paradigm Change of IL-33 in Vascular Biology.International journal of molecular sciences · 2021Review
- Novel role of xanthine oxidase-dependent HRedox biology · 2021Article
- A Novel Plant Leaf Patch Absorbed With IL-33 Antibody Decreases Venous Neointimal hyperplasia.Frontiers in bioengineering and biotechnology · 2021Article
- Role of NFAT in the Progression of Diabetic Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Vascular Health Triad in Humans With Hypertension-Not the Usual Suspects.Frontiers in physiology · 2021Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Objective- IL (interleukin)-33 has been shown to play a role in endothelial dysfunction, but its role in atherosclerosis is controversial. Therefore, the purpose of this study is to examine its role in vascular wall remodeling following injury. Approach and Results- Thrombin induced IL-33 expression in a time-dependent manner in human aortic smooth muscle cells and inhibition of its activity by its neutralizing antibody suppressed thrombin induced human aortic smooth muscle cell migration but not DNA synthesis. In exploring the mechanisms, we found that Par1 (protease-activated receptor 1), Gαq/11 (Gα protein q/11), PLCβ3 (phospholipase Cβ3), NFATc1 (nuclear factor of activated T cells), E2F1 (E2F transcription factor 1), and LMCD1 (LIM and cysteine-rich domains protein 1) are involved in thrombin-induced IL-33 expression and migration. Furthermore, we identified an NFAT-binding site at -100 nt that mediates thrombin-induced IL-33 promoter activity. Interestingly, we observed that NFATc1, E2F1, and LMCD1 bind to NFAT site in response to thrombin and found that LMCD1, while alone has no significant effect, enhanced either NFATc1 or E2F1-dependent IL-33 promoter activity. In addition, we found that guidewire injury induces IL-33 expression in SMC and its neutralizing antibodies substantially reduce SMC migration and neointimal growth in vivo. Increased expression of IL-33 was also observed in human atherosclerotic lesions as compared to arteries without any lesions. Conclusions- The above findings reveal for the first time that thrombin-induced human aortic smooth muscle cell migration and injury-induced neointimal growth require IL-33 expression. In addition, thrombin-induced IL-33 expression requires LMCD1 enhanced combinatorial activation of NFATc1 and E2F1.
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