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J Biomed Biotechnol. 2011;2011:396734. doi: 10.1155/2011/396734. Epub 2011 Feb 9.

Long-term type 1 diabetes enhances in-stent restenosis after aortic stenting in diabetes-prone BB rats.

Author information

1
Section of Immunology, Department of Cell Biology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.

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 (n = 6-7 in each group). Diabetes was suboptimally treated with insulin and was characterized by significant hyperglycaemia, polyuria, proteinuria, and increased HbA(1c) 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.

PMID:
21331346
PMCID:
PMC3038840
DOI:
10.1155/2011/396734
[Indexed for MEDLINE]
Free PMC Article

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