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pubmed-article:18323529pubmed:abstractTextMyocardial infarction, stroke, and venous thromboembolism are characterized by oxygen deprivation. In hypoxia, biological responses are activated that evoke tissue damage. Rapid activation of early growth response-1 in hypoxia upregulates fundamental inflammatory and prothrombotic stress genes. We probed the mechanisms mediating regulation of early growth response-1 and demonstrate that hypoxia stimulates brisk generation of advanced glycation end products (AGEs) by endothelial cells. Via AGE interaction with their chief signaling receptor, RAGE, membrane translocation of protein kinase C-betaII occurs, provoking phosphorylation of c-Jun NH(2)-terminal kinase and increased transcription of early growth response-1 and its downstream target genes. These findings identify RAGE as a master regulator of tissue stress elicited by hypoxia and highlight this receptor as a central therapeutic target to suppress the tissue injury-provoking effects of oxygen deprivation.lld:pubmed
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pubmed-article:18323529pubmed:articleTitleOxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products.lld:pubmed
pubmed-article:18323529pubmed:affiliationDivision of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA.lld:pubmed
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