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Diabetes 51:3311-3317, 2002
© 2002 by the American Diabetes Association, Inc.

STAT5 Activation Induced by Diabetic LDL Depends on LDL Glycation and Occurs Via src Kinase Activity

Maria Felice Brizzi1, Patrizia Dentelli1, Roberto Gambino1, Sara Cabodi2, Maurizio Cassader1, Ada Castelli1, Paola Defilippi2, Luigi Pegoraro1, and Gianfranco Pagano1

1 Department of Internal Medicine, University of Torino, Torino, Italy
2 Department of Genetics, Biology, and biochemistry, University of Torino, Torino, Italy

Advanced glycation end products (AGEs) have been implicated in the accelerated vascular injury occurring in diabetes. We recently reported that LDL prepared from type 2 diabetic patients (dm-LDL), but not normal LDL (n-LDL) triggered signal transducers and activators of transcription STAT5 activation and p21waf expression in endothelial cells (ECs). The aims of the present study were to investigate the role of LDL glycation in dm-LDL- mediated signals and to analyze the molecular mechanisms leading to STAT5 activation. We found that glycated LDL (gly-LDL) triggered STAT5 activation, the formation of a prolactin inducible element (PIE)-binding complex containing STAT5, and increased p21waf expression through the activation of the receptor for AGE (RAGE). We also demonstrated that dm-LDL and gly-LDL, but not n-LDL treatment induced the formation of a stable complex containing the activated STAT5 and RAGE. Moreover, gly-LDL triggered src but not JAK2 kinase activity. Pretreatment with the src kinase inhibitor PP1 abrogated both STAT5 activation and the expression of p21waf induced by gly-LDL. Consistently, gly-LDL failed to activate STAT5 in src-/- fibroblasts. Collectively, our results provide evidence for the role of glycation in dm-LDL-mediated effects and for a specific role of src kinase in STAT5-dependent p21waf expression.


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Copyright © 2002 by the American Diabetes Association.