ArticleAmerican journal of respiratory cell and molecular biology2009
Critical role of serum response factor in pulmonary myofibroblast differentiation induced by TGF-beta.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 107 citations in OpenAlex.
- Mechanosignaling through YAP and TAZ drives fibroblast activation and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2015Trial
- RSK1-SRF signaling axis drives fibroblast activation and pulmonary fibrosis: Genetic causality and therapeutic targeting.iScience · 2026Article
- Cardiac Myofibroblast-Derived Small Extracellular Vesicles Moderate Fibrotic Responses via piRNA-62788/PIWIL2-Mediated SRF Silencing.Journal of extracellular vesicles · 2025Article
- Serum response factor is essential for endometrial function and prevention of inflammatory fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.Molecular pharmacology · 2025Article
- Gα12 and Gα13 proteins are required for transforming growth factor-β-induced myofibroblast differentiation.The Biochemical journal · 2024Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.bioRxiv : the preprint server for biology · 2024Article
- Critical role of Gα12 and Gα13 proteins in TGF-β-induced myofibroblast differentiation.bioRxiv : the preprint server for biology · 2024Article
- Repositioning of ezetimibe for the treatment of idiopathic pulmonary fibrosis.The European respiratory journal · 2024Article
- Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.bioRxiv : the preprint server for biology · 2023Article
- Article
- Myofibroblast-specific inhibition of the Rho kinase-MRTF-SRF pathway using nanotechnology for the prevention of pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Prevention of bleomycin-induced lung fibrosis via inhibition of the MRTF/SRF transcription pathway.Pharmacology research & perspectives · 2022Article
- Mechanical regulation of chromatin and transcription.Nature reviews. Genetics · 2022Review
- Piezo1 Channel as a Potential Target for Hindering Cardiac Fibrotic Remodeling.International journal of molecular sciences · 2022Review
- Anti-fibrotic effects of pharmacologic FGF-2: a review of recent literature.Journal of molecular medicine (Berlin, Germany) · 2022Review
- A single-cell regulatory map of postnatal lung alveologenesis in humans and mice.Cell genomics · 2022Article
- Review
- Computational Methods to Identify Cell-Fate Determinants, Identity Transcription Factors, and Niche-Induced Signaling Pathways for Stem Cell Research.Methods in molecular biology (Clifton, N.J.) · 2022Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) is a cytokine implicated in wound healing and in the pathogenesis of pulmonary fibrosis. TGF-beta stimulates myofibroblast differentiation characterized by expression of contractile smooth muscle (SM)-specific proteins such as SM-alpha-actin. In the present study, we examined the role of serum response factor (SRF) in the mechanism of TGF-beta-induced pulmonary myofibroblast differentiation of human lung fibroblasts (HLF). TGF-beta stimulated SM-alpha-actin expression in HLF, which paralleled with a profound induction of SRF expression and activity. Inhibition of SRF by the pharmacologic SRF inhibitor (CCG-1423), or via adenovirus-mediated transduction of SRF short hairpin RNA (shSRF), blocked the expression of both SRF and SM-alpha-actin in response to TGF-beta without affecting Smad-mediated signaling of TGF-beta. However, forced expression of SRF on its own did not promote SM-alpha-actin expression, whereas expression of the constitutively transactivated SRF fusion protein (SRF-VP16) was sufficient to induce SM-alpha-actin expression, suggesting that both expression and transactivation of SRF are important. Activation of protein kinase A (PKA) by forskolin or iloprost resulted in a significant inhibition of SM-alpha-actin expression induced by TGF-beta, and this was associated with inhibition of both SRF expression and activity, but not of Smad-mediated gene transcription. In summary, this is the first direct demonstration that TGF-beta-induced pulmonary myofibroblast differentiation is mediated by SRF, and that inhibition of myofibroblast differentiation by PKA occurs through down-regulation of SRF expression levels and SRF activity, independent of Smad signaling.
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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.