Abstract
The ubiquitin-proteasome pathway (UPP) plays an important role in regulating gene expression. Retinal pigment epithelial cells (RPE) are a major source of ocular inflammatory cytokines. In this work we determined the relationship between impairment of the UPP and expression of inflammation-related factors. The UPP could be impaired by oxidative stress or chemical inhibition. Impairment of the UPP in RPE increased the expression of several inflammatory cytokines, such as IL-6 and IL-8. However, the expression of monocyte chemoattractant protein-1 (MCP-1) and complement factor H (CFH) and was reduced upon impairment of the UPP. These data suggest that impairment of the UPP in RPE may be one of the causes of retinal inflammation and abnormal functions of monocyte and the complement system during the pathogenesis of age-related macular degeneration.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Cell Line
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Chemokine CCL2 / immunology
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Chemokine CCL2 / metabolism
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Complement Factor H / immunology
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Complement Factor H / metabolism
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Humans
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Interleukin-6 / immunology
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Interleukin-6 / metabolism
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Interleukin-8 / immunology
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Interleukin-8 / metabolism
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Macular Degeneration* / immunology
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Macular Degeneration* / metabolism
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Macular Degeneration* / pathology
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Oxidative Stress / immunology
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Proteasome Endopeptidase Complex / metabolism*
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Retinal Pigment Epithelium / cytology
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Retinal Pigment Epithelium / immunology*
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Retinal Pigment Epithelium / metabolism*
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Retinitis / immunology
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Retinitis / metabolism
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Retinitis / pathology
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Ubiquitin / metabolism*
Substances
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CCL2 protein, human
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CXCL8 protein, human
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Chemokine CCL2
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IL6 protein, human
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Interleukin-6
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Interleukin-8
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Ubiquitin
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Complement Factor H
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Proteasome Endopeptidase Complex