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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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Histology and immunolocalization of cataract  markers. Lenses from ovariectomized rats that received vehicle  alone (A, C, and E) or estrogen  replacement (B, D, and F) were  cultured with 0.15 ng/ml  TGFβ2 and fixed at the end of a  7 d culture period. Serial sections  were stained with haematoxylin  and eosin (A and B), or used for  localization of α-smooth muscle  actin (C and D) and type I collagen (E and F). Lenses from rats  that received vehicle alone developed large anterior subcapsular plaques (A), which contained  spindle-shaped cells (arrow) and  many condensed nuclei. In addition, the fiber cells around the  plaques appeared swollen and  vacuoles were commonly present  (asterisk). α-Smooth muscle actin (C) and type I collagen (E)  were localized within the TGFβinduced subcapsular plaques and  also in some of the cells that remained attached to the capsule  (arrowheads). Lenses from rats that  received estrogen retained normal lens morphology (B) with a  monolayer of epithelial cells (ep)  adjacent to the lens capsule (ca)  and overlying the fibre cells (fc).  These lenses showed no reactivity  for either α-smooth muscle actin  (D) or type I collagen (F). Bar,  40 μm.
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Figure 3: Histology and immunolocalization of cataract markers. Lenses from ovariectomized rats that received vehicle alone (A, C, and E) or estrogen replacement (B, D, and F) were cultured with 0.15 ng/ml TGFβ2 and fixed at the end of a 7 d culture period. Serial sections were stained with haematoxylin and eosin (A and B), or used for localization of α-smooth muscle actin (C and D) and type I collagen (E and F). Lenses from rats that received vehicle alone developed large anterior subcapsular plaques (A), which contained spindle-shaped cells (arrow) and many condensed nuclei. In addition, the fiber cells around the plaques appeared swollen and vacuoles were commonly present (asterisk). α-Smooth muscle actin (C) and type I collagen (E) were localized within the TGFβinduced subcapsular plaques and also in some of the cells that remained attached to the capsule (arrowheads). Lenses from rats that received estrogen retained normal lens morphology (B) with a monolayer of epithelial cells (ep) adjacent to the lens capsule (ca) and overlying the fibre cells (fc). These lenses showed no reactivity for either α-smooth muscle actin (D) or type I collagen (F). Bar, 40 μm.

Mentions: Histologically, the opacities observed in ovariectomized rats that only received vehicle corresponded with subcapsular plaques or clumps of abnormal cells (Fig. 3 A). Reactivity for the cataract markers α-smooth muscle actin and type I collagen was observed predominantly within the subcapsular plaques (Fig. 3, C and E). In contrast, lenses from estrogen-treated rats retained normal cellular morphology (Fig. 3 B), and no reactivity for α-smooth muscle actin or type I collagen was detected (Fig. 3, D and F). In all these respects, lenses from rats that received progesterone replacement were indistinguishable from lenses from rats that received vehicle alone.


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

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

Histology and immunolocalization of cataract  markers. Lenses from ovariectomized rats that received vehicle  alone (A, C, and E) or estrogen  replacement (B, D, and F) were  cultured with 0.15 ng/ml  TGFβ2 and fixed at the end of a  7 d culture period. Serial sections  were stained with haematoxylin  and eosin (A and B), or used for  localization of α-smooth muscle  actin (C and D) and type I collagen (E and F). Lenses from rats  that received vehicle alone developed large anterior subcapsular plaques (A), which contained  spindle-shaped cells (arrow) and  many condensed nuclei. In addition, the fiber cells around the  plaques appeared swollen and  vacuoles were commonly present  (asterisk). α-Smooth muscle actin (C) and type I collagen (E)  were localized within the TGFβinduced subcapsular plaques and  also in some of the cells that remained attached to the capsule  (arrowheads). Lenses from rats that  received estrogen retained normal lens morphology (B) with a  monolayer of epithelial cells (ep)  adjacent to the lens capsule (ca)  and overlying the fibre cells (fc).  These lenses showed no reactivity  for either α-smooth muscle actin  (D) or type I collagen (F). Bar,  40 μm.
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Related In: Results  -  Collection

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Figure 3: Histology and immunolocalization of cataract markers. Lenses from ovariectomized rats that received vehicle alone (A, C, and E) or estrogen replacement (B, D, and F) were cultured with 0.15 ng/ml TGFβ2 and fixed at the end of a 7 d culture period. Serial sections were stained with haematoxylin and eosin (A and B), or used for localization of α-smooth muscle actin (C and D) and type I collagen (E and F). Lenses from rats that received vehicle alone developed large anterior subcapsular plaques (A), which contained spindle-shaped cells (arrow) and many condensed nuclei. In addition, the fiber cells around the plaques appeared swollen and vacuoles were commonly present (asterisk). α-Smooth muscle actin (C) and type I collagen (E) were localized within the TGFβinduced subcapsular plaques and also in some of the cells that remained attached to the capsule (arrowheads). Lenses from rats that received estrogen retained normal lens morphology (B) with a monolayer of epithelial cells (ep) adjacent to the lens capsule (ca) and overlying the fibre cells (fc). These lenses showed no reactivity for either α-smooth muscle actin (D) or type I collagen (F). Bar, 40 μm.
Mentions: Histologically, the opacities observed in ovariectomized rats that only received vehicle corresponded with subcapsular plaques or clumps of abnormal cells (Fig. 3 A). Reactivity for the cataract markers α-smooth muscle actin and type I collagen was observed predominantly within the subcapsular plaques (Fig. 3, C and E). In contrast, lenses from estrogen-treated rats retained normal cellular morphology (Fig. 3 B), and no reactivity for α-smooth muscle actin or type I collagen was detected (Fig. 3, D and F). In all these respects, lenses from rats that received progesterone replacement were indistinguishable from lenses from rats that received vehicle alone.

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