NDLI: Diabetic LDL inhibits cell-cycle progression via STAT5B and p21waf

Content Provider	PubMed Central
Author	Brizzi, Maria Felice Patrizia, Dentelli Pavan, Marzia Rosso, Arturo Gambino, Roberto Cesaris, Maria Grazia De Garbarino, Giovanni Giovanni, Camussi Pagano, Gianfranco Pegoraro, Luigi
Copyright Year	2002
Abstract	Modified LDL is a major cause of injury to the endothelium in diabetes. In the present study, we analyzed the effects on endothelial cells of LDL recovered from type 2 diabetic patients (dm-LDL) or from nondiabetic subjects (n-LDL). Treatment of human umbilical vein endothelial cells with dm-LDL, but not n-LDL, led to the accumulation of cells in G1. To dissect the molecular mechanisms of this effect, we analyzed the expression and function of the cyclin-dependent kinase inhibitor p21waf, a cell cycle regulator known to be a target of the signal transducers and activators of transcription (STATs). dm-LDL led to transient STAT5 phosphorylation and the formation of a STAT5-containing complex and activated p21waf expression at the transcriptional level. Expression of the dominant-negative form of STAT5B, but not of STAT5A, significantly decreased both p21waf expression and the fraction of cells in G1. Finally, immunofluorescence analysis demonstrated that activated STAT5 is expressed in newly formed intraplaque vessels and in endothelial cells lining the luminal side of the plaque. Similarly, p21waf immunoreactivity was found in the neointimal vasculature. Our results suggest a role of STAT5B as a regulator of gene expression in diabetes-associated vascular disease.
Related Links	http://dx.doi.org/10.1172/JCI13617
Starting Page	111
File Format	PDF
ISSN	15588238
e-ISSN	15588238
Journal	The Journal of Clinical Investigation
Issue Number	1
Volume Number	109
Language	English
Publisher	American Society for Clinical Investigation
Publisher Date	2002-01-01
Access Restriction	Open
Rights Holder	American Society for Clinical Investigation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine

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