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Cardiovasc Intervent Radiol. 2012 Dec;35(6):1439-47. doi: 10.1007/s00270-011-0319-3. Epub 2011 Dec 10.

Decreased neointimal extracellular matrix formation in RAGE-knockout mice after microvascular denudation.

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  • 1Department of Diagnostic and Interventional Radiology, University of Tübingen, Hoppe-Seylerstr 3, 72076, Tübingen, Germany.



To evaluate in vivo the role of RAGE (receptor for advanced glycated end products) in the development of restenosis and neointimal proliferation in RAGE-deficient knockout (KO) mice compared with wild-type (WT) mice in an animal model.


Sixteen WT and 15 RAGE-deficient mice underwent microvascular denudation of the common femoral artery under general anaesthesia. Contralateral arteries underwent a sham operation and served as controls. Four weeks after the intervention, all animals were killed, and paraformaldehyde-fixed specimens of the femoral artery were analysed with different stains (hematoxylin and eosin and Elastica van Gieson) and several different types of immunostaining (proliferating cell nuclear antigen, α-actin, collagen, von Willebrand factor, RAGE). Luminal area, area of the neointima, and area of the media were measured in all specimens. In addition, colony-formation assays were performed, and collagen production by WT smooth muscle cells (SMCs) and RAGE-KO SMCs was determined. For statistical analysis, P < 0.05 was considered statistically significant.


Four weeks after denudation, WT mice showed a 49.6% loss of luminal area compared with 14.9% loss of luminal area in RAGE-deficient mice (sham = 0% loss) (P < 0.001). The neointima was 18.2 (*1000 μm(2) [n = 15) in the WT group compared with only 8.4 (*1000 μm(2) [n = 16]) in the RAGE-KO group. RAGE-KO SMCs showed significantly decreased proliferation activity and production of extracellular matrix protein.


RAGE may be shown to play a considerable role in the formation of neointima leading to restenosis after vascular injury.

[PubMed - indexed for MEDLINE]
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