ArticleThe American journal of pathology2006
Matrix metalloproteinase inhibitors suppress transforming growth factor-beta-induced subcapsular cataract formation.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Matrix Metalloproteinases and Their Inhibitors in the Pathogenesis of Epithelial Differentiation, Vascular Disease, Endometriosis, and Ocular Fibrotic Pterygium.International journal of molecular sciences · 2025Review
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
- Unanswered questions regarding the pathogenesis of late onset posterior capsular opacification.Frontiers in ophthalmology · 2025Review
- The Role of Heat Shock Protein 70 (HSP70) in the Pathogenesis of Ocular Diseases-Current Literature Review.Journal of clinical medicine · 2024Review
- Understanding the Role of Yes-Associated Protein (YAP) Signaling in the Transformation of Lens Epithelial Cells (EMT) and Fibrosis.Biomolecules · 2023Article
- Role of Decorin in the Lens and Ocular Diseases.Cells · 2022Review
- The Role of Metalloproteinases and Their Tissue Inhibitors on Ocular Diseases: Focusing on Potential Mechanisms.International journal of molecular sciences · 2022Review
- MMP9 Differentially Regulates Proteins Involved in Actin Polymerization and Cell Migration during TGF-β-Induced EMT in the Lens.International journal of molecular sciences · 2021Article
- Article
- miRNA-26b suppresses the TGF-β2-induced progression of HLE-B3 cellsInternational journal of ophthalmology · 2021Article
- The Protective Effects of Flavonoids in Cataract Formation through the Activation of Nrf2 and the Inhibition of MMP-9.Nutrients · 2020Review
- Expression of transforming growth factor β and matrix metalloproteinases in the aqueous humor of patients with congenital ectopia lentis.Molecular medicine reports · 2019Article
- Investigation of expression and effects of TGF-β1 and MMP-9 in lens epithelial cells of diabetic cataract rats.Experimental and therapeutic medicine · 2019Article
- β-Catenin/Smad3 Interaction Regulates Transforming Growth Factor-β-Induced Epithelial to Mesenchymal Transition in the Lens.International journal of molecular sciences · 2019Article
- Dual function of TGFβ in lens epithelial cell fate: implications for secondary cataract.Molecular biology of the cell · 2017Article
- RhoA/ROCK signaling regulates TGFβ-induced epithelial-mesenchymal transition of lens epithelial cells through MRTF-A.Molecular medicine (Cambridge, Mass.) · 2016Article
- β-Catenin/CBP-Dependent Signaling Regulates TGF-β-Induced Epithelial to Mesenchymal Transition of Lens Epithelial Cells.Investigative ophthalmology & visual science · 2016Article
- Heat shock protein concentration and clarity of porcine lenses incubated at elevated temperatures.Molecular vision · 2016Article
- Aldose Reductase Mediates Transforming Growth Factor β2 (TGF-β2)-Induced Migration and Epithelial-To-Mesenchymal Transition of Lens-Derived Epithelial Cells.Investigative ophthalmology & visual science · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The pleotropic morphogen transforming growth factor-beta (TGFbeta) plays an important role in the development of fibrotic pathologies, including anterior subcapsular cataracts (ASCs). ASC formation involves increased proliferation and transition of lens epithelial cells into myofibroblasts, through epithelial-mesenchymal transformation that results in opaque plaques beneath the lens capsule. In this study, we used a previously established TGFbeta-induced rat cataract model to explore the role of matrix metalloproteinases (MMPs) in ASC formation. Treatment of excised rat lenses with TGFbeta resulted in enhanced secretion of MMP-2 and MMP-9. Importantly, co-treatment with two different MMP inhibitors (MMPIs), the broad spectrum inhibitor GM6001 and an MMP-2/9-specific inhibitor, suppressed TGFbeta-induced ASC changes, including the epithelial-mesenchymal transformation of lens epithelial cells. Using an anti-E-cadherin antibody, we revealed that conditioned media from lenses treated with TGFbeta contained a 72-kd E-cadherin fragment, indicative of E-cadherin shedding. This was accompanied by attenuated levels of E-cadherin mRNA. Conditioned media from lenses co-treated with TGFbeta and MMPIs exhibited attenuated levels of the E-cadherin fragment compared with those from TGFbeta-treated lenses. Together, these findings demonstrate that TGFbeta-induced E-cadherin shedding in the lens is mediated by MMPs and that suppression of this phenomenon might explain the mechanism by which MMPIs inhibit ASC plaque formation.
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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.