ArticleScientific reports2020
Complex fibroblast response to glucocorticoids may underlie variability of clinical efficacy in the vocal folds.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- How post-translational modifications impact glucocorticoid receptor function in human pathologies.Cell communication and signaling : CCS · 2026Review
- Signals of Drug-Related Retinal Fibrosis: Findings From a 20-Year Disproportionality Analysis of Global Spontaneous Reports.Translational vision science & technology · 2026Article
- Novel Molecular Insights into the Anti-Inflammatory and Antifibrotic Effects of Dexamethasone on Human Ligamentum Flavum-Derived Cells.International journal of molecular sciences · 2026Article
- Delineating Effects of Stress-Analogous, Low-Dose Cortisol Exposure on Human Vocal Fold Fibroblasts.Journal of voice : official journal of the Voice Foundation · 2025Article
- Inhibition of the MRTF-A/SRF signaling axis alleviates vocal fold scarring.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- High dose methylprednisolone mediates YAP/TAZ-TEAD in vocal fold fibroblasts with macrophages.Scientific reports · 2025Article
- Concentration Effects of Methylprednisolone in Human Vocal Fold Fibroblast-Macrophage Co-Culture.The Laryngoscope · 2023Article
- Dose-Dependent Glucocorticoid Regulation of Transcription Factors in Vocal Fold Fibroblasts and Macrophages.The Laryngoscope · 2023Article
- Glucocorticoids activate Yes-associated protein in human vocal fold fibroblasts.Experimental cell research · 2021Article
- Mycoplasma affects baseline gene expression and the response to glucocorticoids in vocal fold fibroblasts.Journal of medical microbiology · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Similar to the hypertrophic scar and keloids, the efficacy of glucorticoids (GC) for vocal fold injury is highly variable. We previously reported dexamethasone enhanced the pro-fibrotic effects of transforming growth factor (TGF)-β as a potential mechanism for inconsistent clinical outcomes. In the current study, we sought to determine the mechanism(s) whereby GCs influence the fibrotic response and mechanisms underlying these effects with an emphasis on TGF-β and nuclear receptor subfamily 4 group A member 1 (NR4A1) signaling. Human VF fibroblasts (HVOX) were treated with three commonly-employed GCs+ /-TGF-β1. Phosphorylation of the glucocorticoid receptor (GR:NR3C1) and activation of NR4A1 was analyzed by western blotting. Genes involved in the fibrotic response, including ACTA2, TGFBR1, and TGFBR2 were analyzed by qPCR. RNA-seq was performed to identify global changes in gene expression induced by dexamethasone. GCs enhanced phosphorylation of GR at Ser211 and TGF-β-induced ACTA2 expression. Dexamethasone upregulated TGFBR1, and TGFBR2 in the presence of TGF-β1 and increased active NR4A1. RNA-seq results confirmed numerous pathways, including TGF-β signaling, affected by dexamethasone. Synergistic pro-fibrotic effects of TGF-β were observed across GCs and appeared to be mediated, at least partially, via upregulation of TGF-β receptors. Dexamethasone exhibited diverse regulation of gene expression including NR4A1 upregulation consistent with the anti-fibrotic potential of GCs.
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