ArticleThe Biochemical journal2001
Overexpression of matrix metalloproteinase-2 mediates phenotypic transformation of lens epithelial cells.
Article in The Biochemical journal, 2001. 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, 52 citations in OpenAlex.
- Amelioration of Pulmonary Fibrosis by Matrix Metalloproteinase-2 Overexpression.International journal of molecular sciences · 2023Article
- Article
- Expression of transforming growth factor β and matrix metalloproteinases in the aqueous humor of patients with congenital ectopia lentis.Molecular medicine reports · 2019Article
- Roles of TGF β and FGF Signals in the Lens: Tropomyosin Regulation for Posterior Capsule Opacity.International journal of molecular sciences · 2018Review
- Transforming growth factor beta1 targets estrogen receptor signaling in bronchial epithelial cells.Respiratory research · 2018Article
- FGF2 antagonizes aberrant TGFβ regulation of tropomyosin: role for posterior capsule opacity.Journal of cellular and molecular medicine · 2017Article
- Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2015Review
- Matrix metalloproteinase-9-null mice are resistant to TGF-β-induced anterior subcapsular cataract formation.The American journal of pathology · 2014Article
- Elevated tropomyosin expression is associated with epithelial-mesenchymal transition of lens epithelial cells.Journal of cellular and molecular medicine · 2013Article
- Nuclear translocation of myocardin-related transcription factor-A during transforming growth factor beta-induced epithelial to mesenchymal transition of lens epithelial cells.Molecular vision · 2013Article
- Sprouty is a negative regulator of transforming growth factor β-induced epithelial-to-mesenchymal transition and cataract.Molecular medicine (Cambridge, Mass.) · 2012Article
- Matrix metalloproteinase-2 and -9 activities in the human lens epithelial cells and serum of steroid induced posterior subcapsular cataracts.Molecular vision · 2012Article
- Effect of delivery of MMP inhibitors from PDMS as a model IOL material on PCO markers.Biomaterials · 2010Article
- Protein expression profiling of lens epithelial cells from Prdx6-depleted mice and their vulnerability to UV radiation exposure.American journal of physiology. Cell physiology · 2010Article
- Presence of myofibroblasts and expression of matrix metalloproteinase-2 (MMP-2) in ameloblastomas correlate with rupture of the osseous cortical.Pathology oncology research : POR · 2009Article
- Tissue level, activation and cellular localisation of TGF-beta1 and association with survival in gastric cancer patients.British journal of cancer · 2007Article
- Matrix Metalloproteinases as Mediators of Primary and Secondary Cataracts.Expert review of ophthalmology · 2007Article
- Matrix metalloproteinase inhibitors suppress transforming growth factor-beta-induced subcapsular cataract formation.The American journal of pathology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta (TGF-beta) is known to be a causative factor in pathological fibrosis and the metastasis of cancer cells, through effects on molecules of the extracellular matrix (ECM). We evaluated the influence of TGF-beta(1) on the gene expression of matrix metalloproteinase-2 (MMP-2) in lens epithelial cells (LECs). The results showed that TGF-beta(1) induced the expression of mRNA for MMP-2 in LECs. Subsequently, in order to examine the role of MMP-2, we overexpressed MMP-2 in LECs by stable transfection. The MMP-2-overexpressing LECs showed typical indicators of a myofibroblast-like cell phenotype, such as multiple layers of cells, elongated morphology, and expression of alpha-smooth muscle actin. We also showed that an MMP inhibitor blocked the TGF-beta(1)-induced morphological change in LECs. These results demonstrate that MMP-2 plays a role in the transformation of LECs, which has implications for the pathological fibrosis of these cells.
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