Advanced Glycation End Products and Receptors in Fuchs' Dystrophy Corneas Undergoing Descemet's Stripping with Endothelial Keratoplasty

Zhiyou Wang, James Handa, W. Richard Green, Walter J. Stark, Robert S Weinberg, Albert Jun

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1453-1460
Number of pages8
JournalOphthalmology
Volume114
Issue number8
DOIs
StatePublished - Aug 2007

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Descemet Stripping Endothelial Keratoplasty
Fuchs' Endothelial Dystrophy
Descemet Membrane
Cornea
Corneal Endothelium
Endothelial Cells
Staining and Labeling
Galectin 3
Advanced Glycosylation End Products
Hematoxylin
Eosine Yellowish-(YS)
Advanced Glycosylation End Product-Specific Receptor
Corneal Dystrophy, Fuchs Endothelial, 1
Oxidative Stress
Immunohistochemistry
Outcome Assessment (Health Care)
Apoptosis

ASJC Scopus subject areas

  • Ophthalmology

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Advanced Glycation End Products and Receptors in Fuchs' Dystrophy Corneas Undergoing Descemet's Stripping with Endothelial Keratoplasty. / Wang, Zhiyou; Handa, James; Green, W. Richard; Stark, Walter J.; Weinberg, Robert S; Jun, Albert.

In: Ophthalmology, Vol. 114, No. 8, 08.2007, p. 1453-1460.

Research output: Contribution to journalArticle

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abstract = "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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T1 - Advanced Glycation End Products and Receptors in Fuchs' Dystrophy Corneas Undergoing Descemet's Stripping with Endothelial Keratoplasty

AU - Wang, Zhiyou

AU - Handa, James

AU - Green, W. Richard

AU - Stark, Walter J.

AU - Weinberg, Robert S

AU - Jun, Albert

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N2 - 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.

AB - 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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