RGD Reference Report - Oxidative stress and the regulation of complement activation in human glaucoma. - Rat Genome Database

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Oxidative stress and the regulation of complement activation in human glaucoma.

Authors: Tezel, G  Yang, X  Luo, C  Kain, AD  Powell, DW  Kuehn, MH  Kaplan, HJ 
Citation: Tezel G, etal., Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5071-82. doi: 10.1167/iovs.10-5289. Epub 2010 May 19.
RGD ID: 7364950
Pubmed: PMID:20484586   (View Abstract at PubMed)
PMCID: PMC3066595   (View Article at PubMed Central)
DOI: DOI:10.1167/iovs.10-5289   (Journal Full-text)

PURPOSE: As part of ongoing studies on proteomic alterations during glaucomatous neurodegeneration, this study focused on the complement system. METHODS: Human retinal protein samples obtained from donor eyes with (n = 10) or without (n = 10) glaucoma were analyzed by a quantitative proteomic approach using mass spectrometry. Cellular localization of protein expression for different complement components and regulators were also determined by immunohistochemical analysis of an additional group of human donor eyes with glaucoma (n = 34) compared with age-matched control eyes without glaucoma (n = 20). In addition, to determine the regulation of complement factor H (CFH) by oxidative stress, in vitro experiments were performed using rat retinal cell cultures incubated in the presence and absence of an oxidant treatment. RESULTS: Proteomic analysis detected the expression and differential regulation of several complement components in glaucomatous samples, which included proteins involved in the classical and the lectin pathways of complement activation. In addition, several complement regulatory proteins were detected in the human retinal proteome, and glaucomatous samples exhibited a trend toward downregulation of CFH expression. In vitro experiments revealed that oxidative stress, which was also prominently detectable in the glaucomatous human retinas, downregulated CFH expression in retinal cells. CONCLUSIONS: These findings expand the current knowledge of complement activation by presenting new evidence in human glaucoma and support that despite important roles in tissue cleaning and healing, a potential deficiency in intrinsic regulation of complement activation, as is evident in the presence of oxidative stress, may lead to uncontrolled complement attack with neurodestructive consequences.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CFHHumanglaucoma  IEP protein:decreased expression:retina:RGD 
CfhRatglaucoma  ISOCFH (Homo sapiens)protein:decreased expression:retina:RGD 
CfhMouseglaucoma  ISOCFH (Homo sapiens)protein:decreased expression:retina:RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CfhRatcellular response to hydrogen peroxide  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cfh  (complement factor H)

Genes (Mus musculus)
Cfh  (complement component factor h)

Genes (Homo sapiens)
CFH  (complement factor H)


Additional Information