Literature DB >> 17320180

Advanced glycation end products and receptors in Fuchs' dystrophy corneas undergoing Descemet's stripping with endothelial keratoplasty.

Zhiyou Wang1, James T Handa, W Richard Green, Walter J Stark, Robert S Weinberg, Albert S Jun.   

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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Year:  2007        PMID: 17320180     DOI: 10.1016/j.ophtha.2006.10.049

Source DB:  PubMed          Journal:  Ophthalmology        ISSN: 0161-6420            Impact factor:   12.079


  29 in total

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7.  Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy.

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8.  Decreased DJ-1 leads to impaired Nrf2-regulated antioxidant defense and increased UV-A-induced apoptosis in corneal endothelial cells.

Authors:  Cailing Liu; Yuming Chen; Irene E Kochevar; Ula V Jurkunas
Journal:  Invest Ophthalmol Vis Sci       Date:  2014-07-31       Impact factor: 4.799

9.  Decline in DJ-1 and decreased nuclear translocation of Nrf2 in Fuchs endothelial corneal dystrophy.

Authors:  Maya S Bitar; Cailing Liu; Alireza Ziaei; Yuming Chen; Thore Schmedt; Ula V Jurkunas
Journal:  Invest Ophthalmol Vis Sci       Date:  2012-08-24       Impact factor: 4.799

10.  Protective effect of clusterin on oxidative stress-induced cell death of human corneal endothelial cells.

Authors:  Young Joo Shin; Jeong Hun Kim; Jong Mo Seo; Sang Mok Lee; Joon Young Hyon; Young Suk Yu; Won Ryang Wee
Journal:  Mol Vis       Date:  2009-12-16       Impact factor: 2.367

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