IOVS Molecular Human Reproduction
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(Investigative Ophthalmology and Visual Science. 2006;47:3450-3460.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.05-1208
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Lens-Specific Expression of TGF-ß Induces Anterior Subcapsular Cataract Formation in the Absence of Smad3

Alice Banh,1 Paula A. Deschamps,2 Jack Gauldie,2 Paul A. Overbeek,3 Jacob G. Sivak,1 and Judith A. West-Mays2

1From the School of Optometry, University of Waterloo, Waterloo, Ontario, Canada; the 2Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada; and the 3Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.

PURPOSE. Smad3, a mediator of TGF-ß signaling has been shown to be involved in the epithelial-to-mesenchymal transformation (EMT) of lens epithelial cells in a lens injury model. In this study, the role of Smad3 in anterior subcapsular cataract (ASC) formation was investigated in a transgenic TGF-ß/Smad3 knockout mouse model.

METHODS. TGF-ß1 transgenic mice (containing a human TGF-ß1 cDNA construct expressed under the {alpha}A-crystallin promoter) were bred with mice on a Smad3-null background to generate mice with the following genotypes: TGF-ß1/Smad3–/– (null), TGF-ß1/Smad3+/–, TGF-ß1/Smad3+/+, and nontransgenic/Smad3+/+. Lenses from mice of each genotype were dissected and prepared for histologic or optical analyses.

RESULTS. All transgenic TGF-ß1 lenses demonstrated subcapsular plaque formation and EMT as indicated by the expression of {alpha}-smooth muscle actin. However, the sizes of the plaques were reduced in the TGF-ß1/Smad3–/– lenses, as was the level of type IV collagen deposition when compared with TGF-ß1/Smad3+/– and TGF-ß1/Smad3+/+ lenses. An increased number of apoptotic figures was also observed in the plaques of the TGF-ß1/Smad3–/– lenses compared with TGF-ß1/Smad3+/+ littermates.

CONCLUSIONS. Lens-specific expression of TGF-ß1 induced ASC formation in the absence of the Smad3 signaling mediator, suggests that alternative TGF-ß-signaling pathways participate in this ocular fibrotic model.






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Copyright © 2006 by the Association for Research in Vision and Ophthalmology