May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Wnt Expression in TGFß–induced Cataract Models.
C.C. W. Chong; S.L. Ang; R.J. W. Stump; F.J. Lovicu; J.W. McAvoy
Author Affiliations & Notes
  • C.C. W. Chong
    The Save Sight Institute, University of Sydney, Sydney, Australia
  • S.L. Ang
    The Save Sight Institute, University of Sydney, Sydney, Australia
  • R.J. W. Stump
    The Save Sight Institute, University of Sydney, Sydney, Australia
  • F.J. Lovicu
    The Save Sight Institute, University of Sydney, Sydney, Australia
    The Department of Anatomy and Histology, University of Sydney, Sydney, Australia
  • J.W. McAvoy
    The Save Sight Institute, University of Sydney, Sydney, Australia
    The Department of Anatomy and Histology, University of Sydney, Sydney, Australia
  • Footnotes
    Commercial Relationships  C.C.W. Chong, None; S.L. Ang, None; R.J.W. Stump, None; F.J. Lovicu, None; J.W. McAvoy, None.
  • Footnotes
    Support  NIH Grant EYO3177 and NHMRC (Australia)
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2654. doi:
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      C.C. W. Chong, S.L. Ang, R.J. W. Stump, F.J. Lovicu, J.W. McAvoy; Wnt Expression in TGFß–induced Cataract Models. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2654.

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Abstract

Abstract: : Purpose: Transforming growth factor–beta (TGFß) induces aberrant growth and an epithelial–mesenchymal transition that is characteristic of some forms of human cataract. Besides a direct effect, it is likely that TGFß destabilizes lens cells by disrupting the function of molecules that maintain the normal epithelial phenotype. Recent studies have indicated a role for members of the Wnt growth factor family in formation and maintenance of the lens epithelium. This study investigated the expression of Wnts in established TGFß–induced cataract models. Methods: Wnt expression was examined in two different models of TGFß–induced cataract; whole rat lenses cultured with TGFß or in lenses of transgenic mice that overexpressed TGFß1. For the in vitro studies, whole lenses from postnatal day 21 rats were cultured with and without TGFß2. After 5 days, lenses were microdissected to separate the lens epithelial cells from the fibres. RNA was isolated from these preparations and RT–PCR was conducted using primers for Wnts 5a, 7a and 7b. Lenses were also fixed and prepared for in situ hybridisation (ISH) and immunolocalisation (using a specific antibody for Wnt 5a). For ISH, RNA antisense and sense probes for Wnts 5a, 7a and 7b were prepared with digoxigenin as a label. Results:RT–PCR indicated Wnt5a and Wnt7b were both upregulated and Wnt7b was slightly downregulated in the TGFß2–treated lenses. ISH confirmed these findings and showed that expression was most altered in the cataractous plaques in both whole lens and transgenic mouse models. In addition, there were distinct areas of strong Wnt5a mRNA expression within the cataractous plaques in the transgenic mouse model. Immunolocalisation also showed that Wnt5a protein was strongly expressed in the cataractous plaques in both models, particularly in the cells closest to the lens capsule. In controls, reactivity for Wnt5a protein was present throughout the epithelium and extended into the transitional zone at the lens equator, similar to Wnt5a mRNA expression. Conclusions:Wnt expression is altered in TGFß–induced cataracts. Wnt5a protein and mRNA expression is distinctly upregulated in cataractous plaques. This suggests that Wnt signalling is involved in regulating abnormal growth and differentiation processes in TGFß–induced cataracts.

Keywords: cataract • growth factors/growth factor receptors • gene/expression 
© 2004, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2025 Association for Research in Vision and Ophthalmology.
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