Abstract
Serum levels of advanced glycation end products (AGEs) are associated with an acute phase reactant, C-reactive proteins (CRP) in diabetic patients. However, whether AGEs could directly stimulate hepatic CRP production remains to be elucidated. We found here that AGEs upregulated CRP mRNA levels in cultured Hep3B cells via Rac-1 activation, which was blocked by pigment epithelium-derived factor (PEDF). Our present study suggests that AGEs are one of the potent inducers of CRP and that PEDF may work as an anti-inflammatory agent against AGEs in the liver.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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C-Reactive Protein / biosynthesis*
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C-Reactive Protein / genetics
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Carcinoma, Hepatocellular / enzymology
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / metabolism*
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Carcinoma, Hepatocellular / pathology
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Enzyme Activation / drug effects
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Eye Proteins / pharmacology*
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Gene Expression Regulation, Neoplastic
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Glycation End Products, Advanced / metabolism*
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Humans
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Nerve Growth Factors / pharmacology*
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Phosphoserine / metabolism
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Protein Subunits / metabolism
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RNA, Messenger / genetics
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Reactive Oxygen Species / metabolism
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STAT3 Transcription Factor / metabolism
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Serpins / pharmacology*
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Transcription Factor RelA / metabolism
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rac1 GTP-Binding Protein / genetics
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rac1 GTP-Binding Protein / metabolism*
Substances
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Eye Proteins
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Glycation End Products, Advanced
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Nerve Growth Factors
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Protein Subunits
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RNA, Messenger
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Reactive Oxygen Species
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STAT3 Transcription Factor
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STAT3 protein, human
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Serpins
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Transcription Factor RelA
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pigment epithelium-derived factor
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Phosphoserine
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C-Reactive Protein
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rac1 GTP-Binding Protein