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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 396734, 8 pages
http://dx.doi.org/10.1155/2011/396734
Research Article

Long-Term Type 1 Diabetes Enhances In-Stent Restenosis after Aortic Stenting in Diabetes-Prone BB Rats

1Section of Immunology, Department of Cell Biology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
2Department of Cardiology, Thorax Center, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
3Division of Pathology, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
4Section of Pharmacology and Vascular and Metabolic Disease, Department of Internal Medicine, Erasmus Medical Centre, 3015 CE Rotterdam, The Netherlands

Received 13 September 2010; Revised 9 December 2010; Accepted 4 January 2011

Academic Editor: Monica Fedele

Copyright © 2011 Geanina Onuta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Type 1 diabetic patients have increased risk of developing in-stent restenosis following endovascular stenting. Underlying pathogenetic mechanisms are not fully understood partly due to the lack of a relevant animal model to study the effect(s) of long-term autoimmune diabetes on development of in-stent restenosis. We here describe the development of in-stent restenosis in long-term (~7 months) spontaneously diabetic and age-matched, thymectomized, nondiabetic Diabetes Prone BioBreeding (BBDP) rats ( in each group). Diabetes was suboptimally treated with insulin and was characterized by significant hyperglycaemia, polyuria, proteinuria, and increased HbA1c levels. Stented abdominal aortas were harvested 28 days after stenting. Computerized morphometric analysis revealed significantly increased neointima formation in long-term diabetic rats compared with nondiabetic controls. In conclusion, long-term autoimmune diabetes in BBDP rats enhances in-stent restenosis. This model can be used to study the underlying pathogenetic mechanisms of diabetes-enhanced in-stent restenosis as well as to test new therapeutic modalities.