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© 2001 by the American Diabetes Association, Inc.
Diabetes-Associated Sustained Activation of the Transcription Factor Nuclear Factor-
B
1 Department of Medicine I and Department of Neurology, University of Heidelberg, Heidelberg, Germany
2 Department of Medicine IV, University Tübingen, Tübingen, Germany
3 Department of Anatomy, Department of Immunology, Department of Pathology and Institute of Food Chemistry, Technical University Dresden, Dresden, Germany
4 Department of Laboratory Animal Science, Institute of Pathophysiology, University Greifswald, Karlsburg, Germany
5 Columbia University, Department of Physiology, New York, New York
6 ASTA-Medica, Frankfurt am Main, Germany
7 Institute of Pathology, Case Western Reserve University, Cleveland, Ohio
Activation of the transcription factor nuclear factor-
B (NF-B) has been suggested to participate in chronic disorders, such as diabetes and its complications. In contrast to the short and transient activation of NF-B in vitro, we observed a long-lasting sustained activation of NF-B in the absence of decreased IB
in mononuclear cells from patients with type 1 diabetes. This was associated with increased transcription of NF-Bp65. A comparable increase in NF-Bp65 antigen and mRNA was also observed in vascular endothelial cells of diabetic rats. As a mechanism, we propose that binding of ligands such as advanced glycosylation end products (AGEs), members of the S100 family, or amyloid-ß peptide (Aß) to the transmembrane receptor for AGE (RAGE) results in protein synthesis–dependent sustained activation of NF-B both in vitro and in vivo. Infusion of AGE-albumin into mice bearing a ß-globin reporter transgene under control of NF-B also resulted in prolonged expression of the reporter transgene. In vitro studies showed that RAGE-expressing cells induced sustained translocation of NF-B (p50/p65) from the cytoplasm into the nucleus for >1 week. Sustained NF-B activation by ligands of RAGE was mediated by initial degradation of IB proteins followed by new synthesis of NF-Bp65 mRNA and protein in the presence of newly synthesized IB and IBß. These data demonstrate that ligands of RAGE can induce sustained activation of NF-B as a result of increased levels of de novo synthesized NF-Bp65 overriding endogenous negative feedback mechanisms and thus might contribute to the persistent NF-B activation observed in hyperglycemia and possibly other chronic diseases.
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