The expressions of Fas and caspase-3 in human glaucomatous optic nerve axons
Glaucoma is a chronic neurodegeneration of the optic nerve and one of the leading causes of vision loss in the world among the aging. Recent data suggest an important role for Fas receptor- and caspase-3-mediated apoptosis in the pathophysiology of glaucoma. In this study, Fas receptor and caspase-3...
Saved in:
Published in | Medical science monitor Vol. 14; no. 12; pp. BR274 - BR278 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.12.2008
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Glaucoma is a chronic neurodegeneration of the optic nerve and one of the leading causes of vision loss in the world among the aging. Recent data suggest an important role for Fas receptor- and caspase-3-mediated apoptosis in the pathophysiology of glaucoma. In this study, Fas receptor and caspase-3 immunoexpression in the optic nerve axons of eyeballs with absolute glaucoma and eyes enucleated following extensive trauma were compared.
A series of 25 eyeballs were examined and enucleated during the period of 1994-2005. Seventeen eyeballs were removed from patients with absolute glaucoma who suffered from severe ophthalmalgia and 8 eyeballs were enucleated because of extensive injury on the day of injury or one day thereafter. The samples were obtained from the retrolaminar region of the optic nerve head and evaluated histopathologically. Immunohistochemistry was performed using polyclonal antibodies and the LSAB technique to determine Fas and caspase-3 expression.
The percentages of positive Fas receptor and caspase-3 immunohistochemical staining were higher in the axons with absolute glaucoma than in the trauma group (p=0.0084 for Fas, p=0.0322 for caspase-3).
The results indicate that the apoptosis markers Fas receptor and caspase-3 might play a significant role in glaucoma neuropathy at the stage of absolute glaucoma. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1643-3750 |