ArticleThe Journal of biological chemistry2010
Transforming growth factor-β1 induces expression of human coagulation factor XII via Smad3 and JNK signaling pathways in human lung fibroblasts.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026Pooled it
- RIDDEN: Data-driven inference of receptor activity from transcriptomic data.PLoS computational biology · 2025Article
- Succinate aggravates pulmonary fibrosis through the succinate/SUCNR1 axis.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease.Nature communications · 2024Article
- The impact of inflammation and acute phase activation in cancer cachexia.Frontiers in immunology · 2023Review
- Microvascular significance of TGF-β axis activation in COVID-19.Frontiers in cardiovascular medicine · 2022Review
- The contact system in liver injury.Seminars in immunopathology · 2021Review
- TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review).International journal of molecular medicine · 2021Review
- RGD-binding integrins and TGF-β in SARS-CoV-2 infections - novel targets to treat COVID-19 patients?Clinical & translational immunology · 2021Review
- Article
- Factor XII - What's important but not commonly thought about.Research and practice in thrombosis and haemostasis · 2019Review
- The TGFβ1 Receptor Antagonist GW788388 Reduces JNK Activation and Protects Against Acetaminophen Hepatotoxicity in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Low density lipoprotein receptor-related protein 1 couples β1 integrin activation to degradation.Cellular and molecular life sciences : CMLS · 2018Article
- Factor XII and uPAR upregulate neutrophil functions to influence wound healing.The Journal of clinical investigation · 2018Article
- Down-regulation of USP13 mediates phenotype transformation of fibroblasts in idiopathic pulmonary fibrosis.Respiratory research · 2015Article
- Rapamycin increases CCN2 expression of lung fibroblasts via phosphoinositide 3-kinase.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Heparan sulfate proteoglycans mediate factor XIIa binding to the cell surface.The Journal of biological chemistry · 2015Article
- Custom 4-Plex DiLeu Isobaric Labels Enable Relative Quantification of Urinary Proteins in Men with Lower Urinary Tract Symptoms (LUTS).PloS one · 2015Article
- Advancing the high throughput identification of liver fibrosis protein signatures using multiplexed ion mobility spectrometry.Molecular & cellular proteomics : MCP · 2014Article
- RIP1 potentiates BPDE-induced transformation in human bronchial epithelial cells through catalase-mediated suppression of excessive reactive oxygen species.Carcinogenesis · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coagulation factor XII (FXII) is a liver-derived serine protease involved in fibrinolysis, coagulation, and inflammation. The regulation of FXII expression is largely unknown. Transforming growth factor-beta1 (TGF-beta1) is a multifunctional cytokine that has been linked to several pathological processes, including tissue fibrosis by modulating procoagulant and fibrinolytic activities. This study investigated whether TGF-beta1 may regulate FXII expression in human lung fibroblasts. Treatment of human lung fibroblasts with TGF-beta1 resulted in a time-dependent increase in FXII production, activation of p44/42, p38, JNK, and Akt, and phosphorylation and translocation into the nucleus of Smad3. However, TGF-beta1-induced FXII expression was repressed only by the JNK inhibitor and JNK and Smad3 antisense oligonucleotides but not by MEK, p38, or phosphoinositide 3-kinase blockers. JNK inhibition had no effect on TGF-beta1-induced Smad3 phosphorylation, association with Smad4, and its translocation into the nucleus but strongly suppressed Smad3-DNA complex formation. FXII promoter analysis revealed that the -299/+1 region was sufficient for TGF-beta1 to induce FXII expression. Sequence analysis of this region detected a potential Smad-binding element at position -272/-269 (SBE-(-272/-269)). Chromatin immunoprecipitation and streptavidin pulldown assays demonstrated TGF-beta1-dependent Smad3 binding to SBE-(-272/-269). Mutation or deletion of SBE-(-272/-269) substantially reduced TGF-beta1-mediated activation of the FXII promoter. Clinical relevance was demonstrated by elevated FXII levels and its co-localization with fibroblasts in the lungs of patients with acute respiratory distress syndrome. Our results show that JNK/Smad3 pathway plays a critical role in TGF-beta1-induced FXII expression in human lung fibroblasts and implicate its possible involvement in pathological conditions characterized by elevated TGF-beta1 levels.
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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.