Advanced Glycation End Products and Receptors in Fuchs’ Dystrophy Corneas Undergoing Descemet’s Stripping with Endothelial Keratoplasty
Purpose To describe the histopathologic features of Descemet’s membrane (DM) obtained from Fuchs’ endothelial corneal dystrophy (FECD) corneas undergoing Descemet’s stripping with endothelial keratoplasty (DSEK) and to assess the presence of advanced glycation end products (AGEs) and their receptors...
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Published in | Ophthalmology (Rochester, Minn.) Vol. 114; no. 8; pp. 1453 - 1460 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.08.2007
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Purpose To describe the histopathologic features of Descemet’s membrane (DM) obtained from Fuchs’ endothelial corneal dystrophy (FECD) corneas undergoing Descemet’s stripping with endothelial keratoplasty (DSEK) and to assess the presence of advanced glycation end products (AGEs) and their receptors in FECD endothelium and DM. Design Prospective observational case series. Participants Five eyes of 5 patients undergoing DSEK for FECD and 4 normal control eyebank corneas. Methods Descemet’s membrane and corneal endothelium from FECD patients undergoing DSEK were assessed with hematoxylin–eosin staining and immunohistochemistry for AGEs, receptor of AGEs (RAGE), and galectin 3 (AGE-R3). Main Outcome Measures Histopathologic abnormalities and presence of AGEs, RAGE, and AGE-R3 in DSEK specimens. Results Histopathologic assessment of DSEK specimens from FECD patients disclosed thickening and nodularity of DM and loss of endothelial cells. Immunohistochemical staining of FECD DM for AGE, RAGE, and AGE-R3 showed an abundance of AGEs in the anterior portion of DM, mild positivity for RAGE, and moderate positivity for AGE-R3. Conclusions Tissue quality after DSEK is sufficient to allow detailed histopathologic analysis. The presence of AGEs, RAGE, and AGE-R3 in DM and corneal endothelium of FECD patients supports a link between accumulation of AGEs, oxidative stress, and corneal endothelial cell apoptosis in the pathogenesis of FECD. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0161-6420 1549-4713 |
DOI: | 10.1016/j.ophtha.2006.10.049 |