ArticleThe world journal of men's health2018
Silencing Histone Deacetylase 7 Alleviates Transforming Growth Factor-β1-Induced Profibrotic Responses in Fibroblasts Derived from Peyronie's Plaque.
Article in The world journal of men's health, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Research progress on histone deacetylases in peritoneal dialysis-associated peritoneal fibrosis.Renal failure · 2025Review
- Therapeutic role of histone deacetylase inhibition in anMolecular medicine reports · 2024Article
- Histone deacetylases: potential therapeutic targets for idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Molecular Mechanisms and Risk Factors Related to the Pathogenesis of Peyronie's Disease.International journal of molecular sciences · 2023Review
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- The contribution of the immune system to genitourinary fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- HDAC5-mediated Smad7 silencing through MEF2A is critical for fibroblast activation and hypertrophic scar formation.International journal of biological sciences · 2022Article
- Molecular mechanisms of histone deacetylases and inhibitors in renal fibrosis progression.Frontiers in molecular biosciences · 2022Review
- Histone deacetylase 7 mediates endothelin-1-induced connective tissue growth factor expression in human lung fibroblasts through p300 and activator protein-1 activation.Journal of biomedical science · 2021Article
- New insights into the pathogenesis of Peyronie's disease: A narrative review.Chronic diseases and translational medicine · 2020Review
- Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling.The Journal of clinical investigation · 2020Article
- Peyronie's disease: is it genetic or not?Translational andrology and urology · 2020Review
- TGFβ-induced fibroblast activation requires persistent and targeted HDAC-mediated gene repression.Journal of cell science · 2019Article
- Extracorporeal Shock Wave Therapy in Peyronie's Disease: Clinical Efficacy and Safety from a Single-Arm Observational Study.The world journal of men's health · 2019Article
- Aberrant expression of histone deacetylase 8 in endometriosis and its potential as a therapeutic target.Reproductive medicine and biologyArticle
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10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeEpigenetic modifications, such as histone acetylation/deacetylation and DNA methylation, play a crucial role in the pathogenesis of inflammatory disorders and fibrotic diseases. The aim of this study was to study the differential gene expression of histone deacetylases (HDACs) in fibroblasts isolated from plaque tissue of Peyronie's disease (PD) or normal tunica albuginea (TA) and to examine the anti-fibrotic effect of small interfering RNA (siRNA)-mediated silencing of HDAC7 in fibroblasts derived from human PD plaque. MATERIALS AND
methodsFor differential gene expression study, we performed reverse-transcriptase polymerase chain reaction for HDAC isoforms (1-11) in fibroblasts isolated from PD plaque or normal TA. Fibroblasts isolated from PD plaque were pretreated with HDAC7 siRNA (100 pmol) and then stimulated with transforming growth factor-β1 (TGF-β1, 10 ng/mL). Protein was extracted from treated fibroblasts for Western blotting. We also performed immunocytochemistry to detect the expression of extracellular matrix proteins and to examine the effect of HDAC2 siRNA on the TGF-β1-induced nuclear translocation of Smad2/3 and myofibroblastic differentiation.
resultsThe mRNA expression of HDAC2, 3, 4, 5, 7, 8, 10, and 11 was higher in fibroblasts isolated from PD plaque than in fibroblasts isolated from normal TA tissue. Knockdown of HDAC7 in PD fibroblasts inhibited TGF-β1-induced nuclear shuttle of Smad2 and Smad3, transdifferentiation of fibroblasts into myofibroblasts, and abrogated TGF-β1-induced production of extracellular matrix protein.
conclusionsThese findings suggest that specific inhibition of HDAC7 with RNA interference may represent a promising epigenetic therapy for PD.
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