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Estrogen protects lenses against cataract induced by transforming growth factor-beta (TGFbeta).

Hales AM, Chamberlain CG, Murphy CR, McAvoy JW - J. Exp. Med. (1997)

Bottom Line: Furthermore, lenses from ovariectomized females show increased sensitivity to the damaging effects of TGFbeta and estrogen replacement in vivo, or exposure to estrogen in vitro, restores resistance.The present study in the rat indicates that estrogen provides protection against cataract by countering the damaging effects of TGFbeP.It also adds to an increasing body of evidence that hormone replacement therapy protects postmenopausal women against various diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Histology, and Institute for Biomedical Research (F-13), The University of Sydney, New South Wales, Australia.

ABSTRACT
Cataract, already a major cause of visual impairment and blindness, is likely to become an increasing problem as the world population ages. In a previous study, we showed that transforming growth factor-beta (TGFP) induces rat lenses in culture to develop opacities and other changes that have many features of human subcapsular cataracts. Here we show that estrogen protects against cataract. Lenses from female rats are more resistant to TGFbeta-induced cataract than those from males. Furthermore, lenses from ovariectomized females show increased sensitivity to the damaging effects of TGFbeta and estrogen replacement in vivo, or exposure to estrogen in vitro, restores resistance. Sex-dependent and estrogen-related differences in susceptibility to cataract formation, consistent with a protective role for estrogen, have been noted in some epidemiological studies. The present study in the rat indicates that estrogen provides protection against cataract by countering the damaging effects of TGFbeP. It also adds to an increasing body of evidence that hormone replacement therapy protects postmenopausal women against various diseases.

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Posterior migration of cells associated with induction of cataract by TGFβ. Lenses from ovariectomized rats that received vehicle  alone (A and C) or estrogen replacement (B and D) were cultured with  0.15 ng/ml TGFβ2 and fixed at the end of the 7 d culture period. Serial  sections were stained for routine histology with haematoxylin and eosin  (A and B) or used for immunofluorescent localization of type I collagen  (C and D). The lens equator is positioned at the top of each micrograph.  In lenses from rats that received vehicle alone (A), nucleated cells were  observed migrating along the lens capsule toward the posterior pole (A,  arrowheads). Strong reactivity for type I collagen was associated with these  posteriorly migrating cells (C, arrowheads). In contrast, lenses from rats that  received estrogen replacement maintained a normal lens morphology  with no abnormal migration of cells below the lens equator (B). No reactivity for type I collagen was observed (D). Bar, 40 μm.
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Figure 4: Posterior migration of cells associated with induction of cataract by TGFβ. Lenses from ovariectomized rats that received vehicle alone (A and C) or estrogen replacement (B and D) were cultured with 0.15 ng/ml TGFβ2 and fixed at the end of the 7 d culture period. Serial sections were stained for routine histology with haematoxylin and eosin (A and B) or used for immunofluorescent localization of type I collagen (C and D). The lens equator is positioned at the top of each micrograph. In lenses from rats that received vehicle alone (A), nucleated cells were observed migrating along the lens capsule toward the posterior pole (A, arrowheads). Strong reactivity for type I collagen was associated with these posteriorly migrating cells (C, arrowheads). In contrast, lenses from rats that received estrogen replacement maintained a normal lens morphology with no abnormal migration of cells below the lens equator (B). No reactivity for type I collagen was observed (D). Bar, 40 μm.

Mentions: A variety of more subtle histological changes were observed in lenses from ovariectomized rats that did not receive estrogen. Swelling of cortical fiber cells with evidence of degeneration, reminiscent of cortical cataract (11), was commonly observed (for example see Fig. 3 A), generally in the region of the lens anterior to the equator. In addition, nucleated cells were observed migrating along the posterior capsule towards the posterior pole (Fig. 4 A); these cells showed reactivity for type I collagen (Fig. 4 C), but not for α-smooth muscle actin. None of these changes were observed in lenses from estrogen-treated ovariectomized rats, which remained transparent (Fig. 4, B and D). In lenses from normal male and female rats (not shown), concentrations of TGFβ >0.15 ng/ml were required to induce changes as pronounced as those in Figs. 3 A and 4 A. Thus, lenses from normal rats of either sex seemed to be more resistant to the effects of TGFβ than those from ovariectomized rats that did not receive estrogen.


Estrogen protects lenses against cataract induced by transforming growth factor-beta (TGFbeta).

Hales AM, Chamberlain CG, Murphy CR, McAvoy JW - J. Exp. Med. (1997)

Posterior migration of cells associated with induction of cataract by TGFβ. Lenses from ovariectomized rats that received vehicle  alone (A and C) or estrogen replacement (B and D) were cultured with  0.15 ng/ml TGFβ2 and fixed at the end of the 7 d culture period. Serial  sections were stained for routine histology with haematoxylin and eosin  (A and B) or used for immunofluorescent localization of type I collagen  (C and D). The lens equator is positioned at the top of each micrograph.  In lenses from rats that received vehicle alone (A), nucleated cells were  observed migrating along the lens capsule toward the posterior pole (A,  arrowheads). Strong reactivity for type I collagen was associated with these  posteriorly migrating cells (C, arrowheads). In contrast, lenses from rats that  received estrogen replacement maintained a normal lens morphology  with no abnormal migration of cells below the lens equator (B). No reactivity for type I collagen was observed (D). Bar, 40 μm.
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Related In: Results  -  Collection

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Figure 4: Posterior migration of cells associated with induction of cataract by TGFβ. Lenses from ovariectomized rats that received vehicle alone (A and C) or estrogen replacement (B and D) were cultured with 0.15 ng/ml TGFβ2 and fixed at the end of the 7 d culture period. Serial sections were stained for routine histology with haematoxylin and eosin (A and B) or used for immunofluorescent localization of type I collagen (C and D). The lens equator is positioned at the top of each micrograph. In lenses from rats that received vehicle alone (A), nucleated cells were observed migrating along the lens capsule toward the posterior pole (A, arrowheads). Strong reactivity for type I collagen was associated with these posteriorly migrating cells (C, arrowheads). In contrast, lenses from rats that received estrogen replacement maintained a normal lens morphology with no abnormal migration of cells below the lens equator (B). No reactivity for type I collagen was observed (D). Bar, 40 μm.
Mentions: A variety of more subtle histological changes were observed in lenses from ovariectomized rats that did not receive estrogen. Swelling of cortical fiber cells with evidence of degeneration, reminiscent of cortical cataract (11), was commonly observed (for example see Fig. 3 A), generally in the region of the lens anterior to the equator. In addition, nucleated cells were observed migrating along the posterior capsule towards the posterior pole (Fig. 4 A); these cells showed reactivity for type I collagen (Fig. 4 C), but not for α-smooth muscle actin. None of these changes were observed in lenses from estrogen-treated ovariectomized rats, which remained transparent (Fig. 4, B and D). In lenses from normal male and female rats (not shown), concentrations of TGFβ >0.15 ng/ml were required to induce changes as pronounced as those in Figs. 3 A and 4 A. Thus, lenses from normal rats of either sex seemed to be more resistant to the effects of TGFβ than those from ovariectomized rats that did not receive estrogen.

Bottom Line: Furthermore, lenses from ovariectomized females show increased sensitivity to the damaging effects of TGFbeta and estrogen replacement in vivo, or exposure to estrogen in vitro, restores resistance.The present study in the rat indicates that estrogen provides protection against cataract by countering the damaging effects of TGFbeP.It also adds to an increasing body of evidence that hormone replacement therapy protects postmenopausal women against various diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Histology, and Institute for Biomedical Research (F-13), The University of Sydney, New South Wales, Australia.

ABSTRACT
Cataract, already a major cause of visual impairment and blindness, is likely to become an increasing problem as the world population ages. In a previous study, we showed that transforming growth factor-beta (TGFP) induces rat lenses in culture to develop opacities and other changes that have many features of human subcapsular cataracts. Here we show that estrogen protects against cataract. Lenses from female rats are more resistant to TGFbeta-induced cataract than those from males. Furthermore, lenses from ovariectomized females show increased sensitivity to the damaging effects of TGFbeta and estrogen replacement in vivo, or exposure to estrogen in vitro, restores resistance. Sex-dependent and estrogen-related differences in susceptibility to cataract formation, consistent with a protective role for estrogen, have been noted in some epidemiological studies. The present study in the rat indicates that estrogen provides protection against cataract by countering the damaging effects of TGFbeP. It also adds to an increasing body of evidence that hormone replacement therapy protects postmenopausal women against various diseases.

Show MeSH
Related in: MedlinePlus