ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
EGF antagonizes TGF-beta-induced tropoelastin expression in lung fibroblasts via stabilization of Smad corepressor TGIF.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Epidermal growth factor receptor signaling modulates postoperative pain and inflammatory responses.Frontiers in immunology · 2026Review
- Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis.Antioxidants (Basel, Switzerland) · 2024Review
- Matrix remodeling in chronic lung diseases.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Matrix Remodeling in Pulmonary Fibrosis and Emphysema.American journal of respiratory cell and molecular biology · 2016Review
- A potential role for endogenous proteins as sacrificial sunscreens and antioxidants in human tissues.Redox biology · 2015Article
- Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression.Carcinogenesis · 2015Review
- Epidermal growth factor inhibits transforming growth factor-β-induced fibrogenic differentiation marker expression through ERK activation.Cellular signalling · 2014Article
- JNK suppresses pulmonary fibroblast elastogenesis during alveolar development.Respiratory research · 2014Article
- Crosstalk between Smad and Mitogen-Activated Protein Kinases for the Regulation of Apoptosis in Cyclosporine A- Induced Renal Tubular Injury.Nephron extra · 2011Article
- Protein kinase CK1alphaLS promotes vascular cell proliferation and intimal hyperplasia.The American journal of pathology · 2010Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that neutrophil elastase (NE) downregulates transforming growth factor-beta (TGF-beta)-maintained tropoelastin mRNA levels in lung fibroblasts through transactivation of the epidermal growth factor (EGF) receptor (EGFR)/Mek/Erk pathway, which is dependent on the NE-initiated release of soluble EGFR ligands. In the present study, we investigated the mechanism by which EGF downregulates tropoelastin expression. We found that EGF downregulates tropoelastin expression through inhibition of TGF-beta signaling. We show that EGF does not prevent the TGF-beta-induced nuclear accumulation of Smad2/3; rather, EGF stabilizes the short-lived Smad transcriptional corepressor TG-interacting factor (TGIF) via EGFR/Mek/Erk-mediated phosphorylation of TGIF. Elevation of TGIF levels, either by TGIF overexpression or prevention of TGIF degradation, is sufficient to inhibit TGF-beta-induced tropoelastin expression. Moreover, TGIF is essential for EGF-mediated downregulation of tropoelastin expression, inasmuch as small interfering RNA knockdown of TGIF blocked EGF-induced downregulation of tropoelastin. Finally, we demonstrated that NE treatment, which releases EGF-like growth factors, causes stabilization of TGIF through the EGFR/Mek/Erk pathway. These results suggest that EGFR/Mek/Erk signaling specifically antagonizes the proelastogenic action of TGF-beta in lung fibroblasts by stabilizing the Smad transcriptional corepressor TGIF.
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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.