|
|
||||||||
From the Department of Anatomy and Histology and the Institute for Biomedical Research, The University of Sydney, New South Wales, Australia.
PURPOSE. Cataract is the most common cause of blindness in the world today, and yet there is no generally accepted treatment other than surgical intervention. Studies in rodent models designed to increase understanding of the molecular basis of cataract have shown that transforming growth factor (TGF)-ß induces morphologic and molecular changes similar to those associated with some forms of human cataract. Because aging is the most widely recognized risk factor for cataract, it is important that any animal model be examined in this context. This was a study of the effects of aging on susceptibility to TGFß-induced cataract.
METHODS. Lenses from weanling, adult, and senile rats were cultured in defined serum-free medium with a range of concentrations of TGFß2. The lenses were cultured for up to 7 days, photographed daily, fixed, and prepared for histology and immunolocalization. Opacification was quantified by image analysis.
RESULTS. Lenses from weanling, adult, and senile rats all underwent similar
cataractous changes when exposed to TGFß. This included
opacification, the formation of anterior subcapsular plaques, and
accumulation of type I collagen and
-smooth muscle actin. Lenses
from adult and senile animals, however, were generally more adversely
affected by TGFß than lenses from weanlings. This study also showed
that a low dose of TGFß administered over a prolonged period had an
effect similar to that of a higher dose administered over a shorter
period.
CONCLUSIONS. An elevation of TGFß activity, either acute or chronic, and/or an age-related increase in lens cell susceptibility to TGFß may be triggering factors in the etiology of certain forms of cataract.
This article has been cited by other articles:
![]() |
N. Lois, J. Taylor, A. D. McKinnon, G. C. Smith, R. van't Hof, and J. V. Forrester Effect of TGF-{beta}2 and Anti-TGF-{beta}2 Antibody in a New In Vivo Rodent Model of Posterior Capsule Opacification Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4260 - 4266. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Zhou and A. S. Menko Coordinate Signaling by Src and p38 Kinases in the Induction of Cortical Cataracts Invest. Ophthalmol. Vis. Sci., July 1, 2004; 45(7): 2314 - 2323. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. J. Lovicu, P. Steven, S. Saika, and J. W. McAvoy Aberrant Lens Fiber Differentiation in Anterior Subcapsular Cataract Formation: A Process Dependent on Reduced Levels of Pax6 Invest. Ophthalmol. Vis. Sci., June 1, 2004; 45(6): 1946 - 1953. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Saika, T. Miyamoto, S.-i. Tanaka, T. Tanaka, I. Ishida, Y. Ohnishi, A. Ooshima, T. Ishiwata, G. Asano, T.-i. Chikama, et al. Response of Lens Epithelial Cells to Injury: Role of Lumican in Epithelial-Mesenchymal Transition Invest. Ophthalmol. Vis. Sci., May 1, 2003; 44(5): 2094 - 2102. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Zhou and A. S. Menko The Role of Src Family Kinases in Cortical Cataract Formation Invest. Ophthalmol. Vis. Sci., July 1, 2002; 43(7): 2293 - 2300. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. J Lovicu, M. W Schulz, A. M Hales, L. N Vincent, P. A Overbeek, C. G Chamberlain, and J. W McAvoy TGF{beta} induces morphological and molecular changes similar to human anterior subcapsular cataract Br. J. Ophthalmol., February 1, 2002; 86(2): 220 - 226. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |