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Vol. 179, No. 1-2, 2005
Issue release date: 2005
Section title: Paper
Cells Tissues Organs 2005;179:43–55
(DOI:10.1159/000084508)

Transforming Growth Factor-β-Induced Epithelial-Mesenchymal Transition in the Lens: A Model for Cataract Formation

de Iongh R.U.a · Wederell E.b-e · Lovicu F.J.b-f · McAvoy J.W.b-f
aDepartment of Anatomy and Cell Biology, University of Melbourne, Parkville, and bSave Sight Institute, cDepartment of Clinical Ophthalmology and Eye Health, dDepartment of Anatomy and Histology and eInstitute for Biomedical Research (F13), University of Sydney and fVision CRC, University of New South Wales, Sydney, Australia

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 6/3/2005
Issue release date: 2005

Number of Print Pages: 13
Number of Figures: 7
Number of Tables: 1

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: http://www.karger.com/CTO

Abstract

The vertebrate lens has a distinct polarity and structure that are regulated by growth factors resident in the ocular media. Fibroblast growth factors, in concert with other growth factors, are key regulators of lens fiber cell differentiation. While members of the transforming growth factor (TGFβ) superfamily have also been implicated to play a role in lens fiber differentiation, inappropriate TGFβ signaling in the anterior lens epithelial cells results in an epithelial-mesenchymal transition (EMT) that bears morphological and molecular resemblance to forms of human cataract, including anterior subcapsular (ASC) and posterior capsule opacification (PCO; also known as secondary cataract or after-cataract), which occurs after cataract surgery. Numerous in vitro and in vivo studies indicate that this TGFβ-induced EMT is part of a wound healing response in lens epithelial cells and is characterized by induced expression of numerous extracellular matrix proteins (laminin, collagens I, III, tenascin, fibronectin, proteoglycans), intermediate filaments (desmin, α-smooth muscle actin) and various integrins (α2, α5, α7B), as well as the loss of epithelial genes [Pax6, Cx43, CP49, α-crystallin, E-cadherin, zonula occludens-1 protein (ZO-1)]. The signaling pathways involved in initiating the EMT seem to primarily involve the Smad-dependent pathway, whereby TGFβ binding to specific high affinity cell surface receptors activates the receptor-Smad/Smad4 complex. Recent studies implicate other factors [such as fibroblast growth factor (FGFs), hepatocyte growth factor, integrins], present in the lens and ocular environment, in the pathogenesis of ASC and PCO. For example, FGF signaling can augment many of the effects of TGFβ, and integrin signaling, possibly via ILK, appears to mediate some of the morphological features of EMT initiated by TGFβ. Increasing attention is now being directed at the network of signaling pathways that effect the EMT in lens epithelial cells, with the aim of identifying potential therapeutic targets to inhibit cataract, particularly PCO, which remains a significant clinical problem in ophthalmology.

© 2005 S. Karger AG, Basel


  

Author Contacts

Robb de Iongh
Anatomy and Cell Biology
University of Melbourne
Parkville, Vic. 3010 (Australia)
Tel. +61 3 8344 5788, Fax +61 3 9347 5219, E-Mail r.deIongh@unimelb.edu.au

  

Article Information

Number of Print Pages : 13
Number of Figures : 7, Number of Tables : 1, Number of References : 88

  

Publication Details

Cells Tissues Organs (in vivo, in vitro)

Vol. 179, No. 1-2, Year 2005 (Cover Date: 2005)

Journal Editor: Denker, H.-W. (Essen)
ISSN: 1422–6405 (print), 1422–6421 (Online)

For additional information: http://www.karger.com/cto


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 6/3/2005
Issue release date: 2005

Number of Print Pages: 13
Number of Figures: 7
Number of Tables: 1

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: http://www.karger.com/CTO


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