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Role of extracellular signal-regulated kinase, p38 kinase, and activator protein-1 in transforming growth factor-beta1-induced alpha smooth muscle actin expression in human fetal lung fibroblasts in vitro.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
- Phytochemicals modulating TGF-β signaling in radiation-induced fibrosis.Molecular biology reports · 2026Review
- PIK-III exerts anti-fibrotic effects in activated fibroblasts by regulating p38 activation.PloS one · 2024Article
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- JNK and p38 Inhibitors Prevent Transforming Growth Factor-β1-Induced Myofibroblast Transdifferentiation in Human Graves' Orbital Fibroblasts.International journal of molecular sciences · 2021Article
- The roles of signaling pathways in SARS-CoV-2 infection; lessons learned from SARS-CoV and MERS-CoV.Archives of virology · 2021Review
- Hypoxia-Induced Epithelial-To-Mesenchymal Transition Mediates Fibroblast Abnormalities via ERK Activation in Cutaneous Wound Healing.International journal of molecular sciences · 2019Article
- Concise Review: Therapeutic Potential of the Mesenchymal Stem Cell Derived Secretome and Extracellular Vesicles for Radiation-Induced Lung Injury: Progress and Hypotheses.Stem cells translational medicine · 2019Review
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Role of Bone Morphogenetic Protein 7 (BMP7) in the Modulation of Corneal Stromal and Epithelial Cell Functions.International journal of molecular sciences · 2018Article
- Hypoxia Inducible Factor (HIF) Hydroxylases as Regulators of Intestinal Epithelial Barrier Function.Cellular and molecular gastroenterology and hepatology · 2017Review
- Targeting of Discoidin Domain Receptor 2 (DDR2) Prevents Myofibroblast Activation and Neovessel Formation During Pulmonary Fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Active transforming growth factor-β is associated with phenotypic changes in granulomas after drug treatment in pulmonary tuberculosis.Fibrogenesis & tissue repair · 2016Article
- Atrial Fibrillation and Fibrosis: Beyond the Cardiomyocyte Centric View.BioMed research international · 2015Review
- Inhibition of transglutaminase 2, a novel target for pulmonary fibrosis, by two small electrophilic molecules.American journal of respiratory cell and molecular biology · 2014Article
- The epithelium in idiopathic pulmonary fibrosis: breaking the barrier.Frontiers in pharmacology · 2014Review
- Connective tissue disorders and cardiovascular complications: the indomitable role of transforming growth factor-beta signaling.Advances in experimental medicine and biology · 2014Review
- Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis.Biochimica et biophysica acta · 2013Article
- Schistosoma japonicum egg antigen up-regulates fibrogenesis and inhibits proliferation in primary hepatic stellate cells in a concentration-dependent manner.World journal of gastroenterology · 2013Article
- P190B RhoGAP overexpression in the developing mammary epithelium induces TGFβ-dependent fibroblast activation.PloS one · 2013Article
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Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofibroblasts characterized by alpha smooth muscle actin(alpha-SMA) expression play a key role in pulmonary fibrosis. Transforming growth factor-beta1 (TGF-beta1) is likely to be involved in the emergence of myofibroblasts, but the intracellular signal pathways for this process have not been well determined. The aim of the present study was to investigate the role of mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathways in TGF-beta1-induced alpha-SMA expression in human fetal lung fibroblasts (HLF-02). We found that TGF-beta1 treatment activated p38 kinase and extracellular signal-regulated kinase (Erk) in HLF-02 cells. The induction of alpha-SMA by TGF-beta1 was suppressed by p38 kinase inhibitor (SB203580) and Erk inhibitor (PD98059). AP-1 inhibitor curcumin also inhibited TGF-beta1-induced alpha-SMA expression. In addition, dominant negative mutant c-Jun (TAM67) downregulated TGF-beta1-induced AP-1 transactivation and alpha-SMA expression. In additional, PD98059 but not SB203580 inhibited the AP-1 DNA binding activity induced by TGF-beta1. Based on these findings, we conclude that p38 kinase, Erk, and AP-1 are responsible for the alpha-SMA expression induced by TGF-beta1 in human fetal lung fibroblasts. Erk is involved in inducing alpha-SMA expression via AP-1 activation.
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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.