ArticleMolecular vision2010
Suppression of injury-induced epithelial-mesenchymal transition in a mouse lens epithelium lacking tenascin-C.
Article in Molecular vision, 2010. 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, 27 citations in OpenAlex.
- Unanswered questions regarding the pathogenesis of late onset posterior capsular opacification.Frontiers in ophthalmology · 2025Review
- Sulfur mustard corneal injury is associated with alterations in the epithelial basement membrane and stromal extracellular matrix.Experimental and molecular pathology · 2022Article
- Lens Fibrosis: Understanding the Dynamics of Cell Adhesion Signaling in Lens Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2022Review
- Fibrosis: Shared Lessons From the Lens and Cornea.Anatomical record (Hoboken, N.J. : 2007) · 2020Review
- Adducins inhibit lung cancer cell migration through mechanisms involving regulation of cell-matrix adhesion and cadherin-11 expression.Biochimica et biophysica acta. Molecular cell research · 2019Article
- Roles of TGF β and FGF Signals in the Lens: Tropomyosin Regulation for Posterior Capsule Opacity.International journal of molecular sciences · 2018Review
- Tropomyosin 2 heterozygous knockout in mice using CRISPR-Cas9 system displays the inhibition of injury-induced epithelial-mesenchymal transition, and lens opacity.Mechanisms of ageing and development · 2018Article
- The murine lens: A model to investigate in vivo epithelial-mesenchymal transition.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Review
- Transcriptome of the GSH-Depleted Lens Reveals Changes in Detoxification and EMT Signaling Genes, Transport Systems, and Lipid Homeostasis.Investigative ophthalmology & visual science · 2017Article
- Tenascins in fibrotic disorders-from bench to bedside.Cell adhesion & migration · 2015Review
- Tenascin C in metastasis: A view from the invasive front.Cell adhesion & migration · 2015Review
- The roles of αV integrins in lens EMT and posterior capsular opacification.Journal of cellular and molecular medicine · 2014Article
- Attenuation of human lens epithelial cell spreading, migration and contraction via downregulation of the PI3K/Akt pathway.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014Article
- The correlation between tenascin-C expression, and formation of intestinal stricture.Northern clinics of Istanbul · 2014Article
- Tenascin C promiscuously binds growth factors via its fifth fibronectin type III-like domain.PloS one · 2013Article
- How do tenascins influence the birth and life of a malignant cell?Journal of cellular and molecular medicine · 2012Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the role of tenascin-C in epithelial-mesenchymal transition (EMT) of the lens epithelium during wound healing in mice. Tenascin-C is a component of the extracellular matrix in patients having post-operative capsular opacification.
methodsThe crystalline lens was injured by needle puncture in tenascin-C null (KO, n=56) and wild-type (WT, n=56) mice in a C57BL/6 background. The animals were killed at day 2, 5, or 10 post-injury. Immunohistochemistry was employed to detect alpha-smooth muscle actin (alphaSMA), a marker of EMT, collagen type I, transforming growth factor beta1 (TGFbeta1), phospho-Smad2, phospho-adducin, and phospho-myosin light chain 9 (MLC9). The expression levels of phospho-adducin and phospho-MLC9 were used as markers for the activation of protein kinase C and Rho kinase, respectively.
resultsThe expression of tenascin-C was upregulated in WT lens epithelial cells adjacent to the capsular break at day 5. The results showed that injury-induced EMT of the mouse lens epithelium, as evaluated by histology and the expression patterns of alphaSMA and fibronectin, was attenuated in the absence of tenascin-C. Upregulation of TGFbeta1 expression in the epithelium was also inhibited, and loss of tenascin-C attenuated the phosphorylation of Smad2 and adducin in epithelial cells adjacent to the capsular break. The expression of phospho-adducin was suppressed, while the expression level of phospho-MLC9 was unchanged, in the healing epithelium in the absence of tenascin C.
conclusionsTenascin-C is required for injury-induced EMT in the mouse lens epithelium. The mechanism behind this might involve impaired activation of cytoplasmic signaling cascades; i.e., TGFbeta/Smad and protein kinase C-adducing signaling, in the absence of tenascin-C.
Indexed as
Identifiers
20664686PMC2901186W2157782417What OpenQuestion holds
Registered trials
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.