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Cardiovascular Research Advance Access first published online on July 25, 2009
This version [Corrected Proof] published online on August 12, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp262
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

A novel mouse model of in situ stenting

Janet Chamberlain1,*, Mark Wheatcroft1, Nadine Arnold1, Henry Lupton2, David C. Crossman1, Julian Gunn1,{dagger} and Sheila Francis1,{dagger}

1 Department of Cardiovascular Science, School of Medicine and Biomedical Sciences, Floor L, Medical School, Beech Hill Road, Sheffield S10 2RX, UK
2 Brivant Medical Engineering, Galway, Ireland

* Corresponding author. Tel: +44 114 2713696, Fax: +44 114 2268898, Email: j.chamberlain{at}sheffield.ac.uk

Aims: Animal models of stenting are mostly limited to larger animals or involve substantial abdominal surgery in rodents. We aimed to develop a simple, direct model of murine stenting.

Methods and results: We designed a miniature, self-expanding, nitinol wire coil stent that was pre-loaded into a metal stent sheath. This was advanced into the abdominal aorta of the mouse, via femoral access, and the stent deployed. In-stent restenosis was investigated at 1, 3, 7, and 28 days post-stenting. The model was validated by investigation of neointima formation in mice deficient in signalling via the interleukin-1 receptor (IL-1R1), compared with other injury models. Ninety-two per cent of mice undergoing the procedure were successfully stented. All stented vessels were patent. Inflammatory cells were seen in the adventitia and around the stent strut up to 3 days post-stenting. At 3 days, an early neointima was present, building to a mature neointima at 28 days. In mice lacking IL-1R1, the neointima was 64% smaller than that in wild-type controls at the 28-day timepoint, in agreement with other models.

Conclusion: This is the first description of a successful model of murine in situ stenting, using a stent specifically tailored for use in small thin-walled arteries. The procedure can be undertaken by a single operator without the need for an advanced level of microsurgical skill and is reliable and reproducible. The utility of this model is demonstrated by a reduction in in-stent restenosis in IL-1R1-deficient mice.

KEYWORDS Mouse stent model

Time for primary review: 14 days

{dagger} These two individuals are joint senior authors.


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