Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products.

@article{citeulike:3280792, abstract = {Myocardial 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.}, address = {Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA.}, author = {Chang, J. S. and Wendt, T. and Qu, W. and Kong, L. and Zou, Y. S. and Schmidt, A. M. and Yan, S. F. }, citeulike-article-id = {3280792}, doi = {http://dx.doi.org/10.1161/CIRCRESAHA.107.165308}, issn = {1524-4571}, journal = {Circulation research}, keywords = {egr1, hypoxia, rage}, month = {April}, number = {8}, pages = {905--913}, posted-at = {2008-09-17 16:29:55}, priority = {2}, title = {Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products.}, url = {http://dx.doi.org/10.1161/CIRCRESAHA.107.165308}, volume = {102}, year = {2008} }

TY - JOUR ID - citeulike:3280792 L3 - citeulike-article-id:3280792 N2 - Myocardial 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. IS - 8 JF - Circulation research SN - 1524-4571 AD - Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA. EP - 913 TI - Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products. VL - 102 SP - 905 KW - egr1 KW - hypoxia KW - rage AU - Chang, JS AU - Wendt, T AU - Qu, W AU - Kong, L AU - Zou, YS AU - Schmidt, AM AU - Yan, SF PY - 2008/04/25/ UR - http://dx.doi.org/10.1161/CIRCRESAHA.107.165308 ER -