ArticleMolecular medicine (Cambridge, Mass.)2021
TGF-β-induced α-SMA expression is mediated by C/EBPβ acetylation in human alveolar epithelial cells.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
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- Pulmonary fibrosis in post-COVID-19: epithelial-mesenchymal transition as a key mechanism and target for therapy.Inflammopharmacology · 2026Review
- Perifollicular Lymphocytic Inflammation and Fibrosis in Dissecting Cellulitis: Evidence of a Consistent Histopathologic Pattern.Clinical, cosmetic and investigational dermatology · 2026Article
- Rewired DDR-TGF-β-β-catenin-PD-L1 axis accelerates progression and shapes therapy in human papillomavirus-driven cancer.Frontiers in immunology · 2026Review
- Single-cell RNA sequencing reveals a pro-fibrotic epithelial subpopulation contributing to endometrial dysfunction in polycystic ovary syndrome.Frontiers in endocrinology · 2026Article
- Microbial Monotherapy With Leuconostoc sp LB-P8 Improves Inflammation and Fibrosis in Mouse Primary Sclerosing Cholangitis by Inhibiting Transforming Growth Factor β1/SMAD Signaling.Cellular and molecular gastroenterology and hepatology · 2026Article
- Perifollicular Inflammation and Fibrosis in Androgenetic Alopecia: Implications for Diagnosis and Treatment - A Comparative Histopathologic and Clinical Study with Normal-Appearing Scalp.Clinical, cosmetic and investigational dermatology · 2026Article
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Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the morbidity and mortality rates associated with idiopathic pulmonary fibrosis (IPF) are high, there is still lack of powerful and precise therapeutic options for IPF. OBJECT: Through in vitro model, this study sought to determine whether binding of acetylated CCAAT/enhancer binding protein β (C/EBPβ) to alpha-smooth muscle actin (α-SMA) promoter could affect the activity of the latter as well as assess if it is essential for epithelial-to-mesenchymal transition (EMT) and extracellular matrix deposition in IPF.
methodsThe expression of EMT and C/EBPβ in A549 cells treated with transforming growth factor-beta (TGF-β) as pulmonary fibrotic model was detected by western blotting and qPCR. Collagen-I expression using ELISA was performed. The luciferase activity was used to examine the activity of C/EBPβ. Knockdown of C/EBPβ was performed by siRNA. We also investigated the effect of deacetylation of C/EBPβ on EMT using sirtuin 1 (SIRT1). The binding ability of C/EBPβ with α-SMA promoter was affirmed via chromatin immunoprecipitation (ChIP) and electrophoresis mobility shift assay (EMSA). The relationship between α-SMA and acetylated C/EBPβ was determined with co-immunoprecipitation (Co-IP). SiRNA-mediated knockdown of C/EBPβ in A549 cells attenuated TGF-β1-induced myofibroblast differentiation and ECM deposition. The extent of association between acetylated C/EBPβ and α-SMA promoter was dynamically monitored.
resultsIt was confirmed that deacetylation of C/EBPβ in A549 cells successfully ameliorated TGF-β1-induced EMT, as shown by reduction in α-SMA expression and excessive collagen-I accumulation.
conclusionThe EMT and fibrotic effect of TGF-β1 is dependent on acetylated C/EBPβ-mediated regulation of α-SMA gene activity. Thus, C/EBPβ acetylation may play a central role in pulmonary fibrosis.
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