ArticleThe Laryngoscope2016
The role of Smad3 in the fibrotic phenotype in human vocal fold fibroblasts.
Article in The Laryngoscope, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- TGF-β1 Induced Methylation to Regulate SOCS3 Expression in Abnormal Activation of Vocal Fold Fibroblasts.World journal of otorhinolaryngology - head and neck surgery · 2026Article
- Controlled decorin delivery from injectable microgels promotes scarless vocal fold repair.bioRxiv : the preprint server for biology · 2025Article
- SOCS3 Silencing Promotes Activation of Vocal Fold Fibroblasts via JAK2/STAT3 Signaling Pathway.Inflammation · 2023Article
- Scalable and High-Throughput In Vitro Vibratory Platform for Vocal Fold Tissue Engineering Applications.Bioengineering (Basel, Switzerland) · 2023Article
- PDGFBB improved the biological function of menstrual blood-derived stromal cells and the anti-fibrotic properties of exosomes.Stem cell research & therapy · 2023Article
- 3D collagen migration patterns reveal a SMAD3-dependent and TGF-β1-independent mechanism of recruitment for tumour-associated fibroblasts in lung adenocarcinoma.British journal of cancer · 2023Article
- Concurrent YAP/TAZ and SMAD signaling mediate vocal fold fibrosis.Scientific reports · 2021Article
- Article
- Porcine Vocal Fold Lamina Propria-Derived Biomaterials Modulate TGF-β1-Mediated Fibroblast Activation in Vitro.ACS biomaterials science & engineering · 2020Article
- Implementing Efficient Peptoid-Mediated Delivery of RNA-Based Therapeutics to the Vocal Folds.Laryngoscope investigative otolaryngology · 2019Article
- Pathophysiology of Fibrosis in the Vocal Fold: Current Research, Future Treatment Strategies, and Obstacles to Restoring Vocal Fold Pliability.International journal of molecular sciences · 2019Review
- Phosphorylation of the glucocorticoid receptor alters SMAD signaling in vocal fold fibroblasts.The Laryngoscope · 2019Article
- The effects of cytosporone-B, a novel antifibrotic agent, on vocal fold fibroblasts.The Laryngoscope · 2018Article
- Nanoparticle delivery of RNA-based therapeutics to alter the vocal fold tissue response to injury.The Laryngoscope · 2018Article
- NR4A1 is an endogenous inhibitor of vocal fold fibrosis.The Laryngoscope · 2017Article
- SMAD3 expression and regulation of fibroplasia in vocal fold injury.The Laryngoscope · 2017Article
- Stem Cell-Mediated Paracrine Signaling Alters Fibroplasia in Human Vocal Fold Fibroblasts in Vitro.The Annals of otology, rhinology, and laryngology · 2017Article
- Preliminary study of a novel transfection modality for in vivo siRNA delivery to vocal fold fibroblasts.The Laryngoscope · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectives/hypothesisTo investigate the role of Smad3 as a regulator of transforming growth factor (TGF)-β1-mediated cell activities associated with fibrosis in normal human vocal fold fibroblasts. We also sought to confirm the temporal stability of Smad3 knockdown via small inhibitor ribonucleic acid (siRNA). Vocal fold fibroblasts were employed to determine the effects of Smad3 knockdown on TGF-β1-mediated migration and contraction, as well as regulation of connective tissue growth factor (CTGF). We hypothesized that Smad3 is an ideal candidate for therapeutic manipulation in vivo based on its role in fibrosis. STUDY
designIn vitro.
methodsKnockdown of Smad3 via siRNA was performed in our normal human vocal fold cell line. Three-dimensional collagen gel contraction and scratch assays were employed to determine the role of Smad3 on TGF-β1-mediated contraction and migration, respectively. The role Smad3 in the induction of CTGF was characterized via sodium dodecyl sulfate polyacrylamide gel electrophoresis. The effects of Smad3 signaling on Smad7 messenger (m)RNA and protein were also quantified.
resultsSmad3 knockdown was temporally-stable up to 72 hours (P < 0.001), diminished TGF-β1-mediated collagen gel contraction and migration, and blunted induction of CTGF, but it had no effect on TGF-β1-mediated Smad7 mRNA or protein induction.
conclusionTransforming growth factor-β1 stimulated profibrotic cell activities in our cell line and these actions were largely reduced with Smad3 knockdown. These data provide continued support for therapeutic targeting of Smad3 for vocal fold fibrosis because it appears to regulate the fibrotic phenotype. LEVEL OF EVIDENCE: N/A. Laryngoscope, 126:1151-1156, 2016.
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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.