ArticleInternational journal of ophthalmology2023
17β-estradiol inhibits TGF-β-induced collagen gel contraction mediated by human Tenon fibroblasts
Article in International journal of ophthalmology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- An enhanced-permeability amphiphilic nanogel loaded with sulforaphane for synergistic anti-oxidative and anti-ferroptotic therapy of corneal alkali burn.Journal of translational medicine · 2026Article
- Estrogen signaling processes in fibroblasts: a scoping review.Frontiers in endocrinology · 2026Article
- ECM Remodeling in Direct Inguinal Hernia: The Role of Aging, Oxidative Stress, and Antioxidants Defenses.Clinics and practice · 2025Review
- Semaphorin 7A impairs barrier function in cultured human corneal epithelial cells in a manner dependent on nuclear factor-kappa B.International journal of ophthalmology · 2024Article
- Potential of the Novel Slot Blot Method with a PVDF Membrane for Protein Identification and Quantification in Kampo Medicines.Membranes · 2023Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the impact of 17β-estradiol on the collagen gels contraction (CGC) and inflammation induced by transforming growth factor (TGF)-β in human Tenon fibroblasts (HTFs).
methodsHTFs were three-dimensionally cultivated in type I collagen-generated gels with or without TGF-β (5 ng/mL), 17β-estradiol (12.5 to 100 µmol/L), or progesterone (12.5 to 100 µmol/L). Then, the collagen gel diameter was determined to assess the contraction, and the development of stress fibers was analyzed using immunofluorescence staining. Immunoblot and gelatin zymography assays were used to analyze matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) being released into culture supernatants. Enzyme-linked immunosorbent assay (ELISA) and reverse transcription-quantitative polymerase chain reaction (RT-PCR) were used to detect interleukin (IL)-6, monocyte chemoattractant proteins (MCP)-1, and vascular endothelial growth factor (VEGF) in HTFs at the translational and transcriptional levels. The phosphorylation levels of Sma- and Mad-related proteins (Smads), mitogen-activated protein kinases (MAPKs), and protein kinase B (AKT) were measured by immunoblotting. Statistical analysis was performed using either the Tukey-Kramer test or Student's unpaired
resultsThe CGC caused by TGF-β in HTFs was significantly inhibited by 17β-estradiol (25 to 100 µmol/L), and a statistically significant difference was observed when comparing the normal control group with 17β-estradiol concentrations exceeding 25 µmol/L (
conclusion17β-estradiol significantly inhibits the CGC and inflammation caused by TGF-β in HTFs. This inhibition is likely related to the suppression of stress fibers, inhibition of MMPs, and attenuation of Smads and MAPK (ERK and p38) signaling. 17β-estradiol may have potential clinical benefits in preventing scar development and inflammation in the conjunctiva.
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