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A mouse model to assess neointimal formation following endothelial denudation and bioresorbable stent implantation (671.12)
Author(s) -
Nehzati Ashkon,
Davalian Dariush,
Magana Jesus,
Consigny Paul,
Cardinal Trevor
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.671.12
Subject(s) - restenosis , medicine , stent , abdominal aorta , thrombosis , bare metal stent , cardiology , aorta , radiology , surgery , drug eluting stent
Restenosis is a common response to bare‐metal stent implantation occurring in 16‐44% of patients. Drug‐eluting stents can reduce restenosis, but late‐stent thrombosis occurs in 0.4‐0.6% of patients following cessation of anti‐platelet therapy. Bioresorbable stents may limit both restenosis and late thrombosis. The goal of this work is to develop a mouse model that can be used to assess neointimal formation in response to injury and/or bioresorbable stent implantation. The endothelium was denuded in the abdominal aorta of C57Bl/6 mice using a nitinol device inserted into the femoral artery and confirmed using Evans Blue staining and histopathology. Bioresorbable stent implantation was performed by placing a stent (polymeric coil) in a PE tube, and advancing it into the abdominal aorta. Using a wire advancer, the stent was placed while withdrawing the tube simultaneously. Staining and histopathology revealed endothelial denudation of the abdominal aorta between the renal arteries and iliac bifurcation during acute procedures and increases in wall thickness and cellularity over 28 days. Direct visualization revealed that the polymeric stent can be delivered to area of endothelial denudation with no migration or distal embolization. In summary, we created a mouse model to assess neointimal formation following endothelial denudation and/or bioresorbable stent deployment. In the future, this model can be used to characterize gene expression and assess specific molecular pathways that contribute to restenosis and thrombosis.