Abstract
Diabetic retinopathy is a chronic low-grade inflammatory disease; however, the mechanisms remain elusive. In the present study, we demonstrated that endoplasmic reticulum (ER) stress was activated in the retina in animal models of diabetes and oxygen-induced retinopathy (OIR). Induction of ER stress by tunicamycin resulted in significantly increased expression of inflammatory molecules in the retina. Inhibition of ER stress by chemical chaperone 4-phenyl butyric acid ameliorated inflammation in cultured human retinal endothelial cells exposed to hypoxia, and in the retinas of diabetic and OIR mice. These findings indicate that ER stress is a potential mediator of retinal inflammation in diabetic retinopathy.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Cells, Cultured
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DNA Primers
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Diabetic Retinopathy / metabolism*
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Endoplasmic Reticulum / metabolism*
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Endoplasmic Reticulum Chaperone BiP
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Endoribonucleases / metabolism
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Eukaryotic Initiation Factor-2 / metabolism
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Heat-Shock Proteins / metabolism
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Humans
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Immunohistochemistry
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Mice
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Mice, Inbred C57BL
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Molecular Chaperones / metabolism
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Oxidative Stress* / drug effects
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Phenylbutyrates / pharmacology
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Protein Serine-Threonine Kinases / metabolism
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Retina / metabolism
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Retinitis / metabolism*
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Necrosis Factor-alpha / metabolism
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Tunicamycin / pharmacology
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Vascular Endothelial Growth Factor A / metabolism
Substances
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DNA Primers
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Endoplasmic Reticulum Chaperone BiP
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Eukaryotic Initiation Factor-2
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Heat-Shock Proteins
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Molecular Chaperones
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Phenylbutyrates
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Tumor Necrosis Factor-alpha
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Vascular Endothelial Growth Factor A
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Tunicamycin
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4-phenylbutyric acid
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Ern1 protein, mouse
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Protein Serine-Threonine Kinases
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Endoribonucleases