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Development of a total atherosclerotic occlusion with cell‐mediated calcium deposits in a rabbit femoral artery using tissue‐engineering scaffolds
Author(s) -
Zhu Beili,
Bailey Steven R.,
Elliott James,
Li Xiankai,
Escobar G. Patricia,
Rodriguez Eva M.,
Agrawal C. Mauli
Publication year - 2012
Publication title -
journal of tissue engineering and regenerative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.835
H-Index - 72
eISSN - 1932-7005
pISSN - 1932-6254
DOI - 10.1002/term.413
Subject(s) - calcium , occlusion , femoral artery , medicine , chemistry , biomedical engineering , anatomy , surgery
This study sought to establish a chronic total occlusion (CTO) model with cell‐mediated calcium deposits in rabbit femoral arteries. CTO is the most severe case in atherosclerosis and contains calcium deposits. Previous animal models of CTO do not mimic the gradual occlusion of arteries or have calcium in physiological form. In the present study we tested the strategy of placing tissue‐engineering scaffolds preloaded with cells in arteries to develop a novel CTO model. Primary human osteoblasts (HOBs) were first cultured in vitro on polycaprolactone (PCL) scaffolds with 5 ng TGFβ1 loading for 28 days for precalcification. The HOB–PCL construct was then implanted into a rabbit femoral artery for an additional 3, 10 or 28 days. At the time of sacrifice, angiograms and gross histology of arteries were captured to examine the occlusion of arteries. Fluorescent staining of calcium and EDS detection of calcium were used to evaluate the presence and distribution of calcium inside arteries. Rabbit femoral arteries were totally occluded over 28 days. Calcium was presented at CTO sites at 3, 10 and 28 days, with the day 10 specimens showing the maximum calcium. Chronic inflammatory response and recanalization were observed in day 28 CTO sites. A novel CTO model with cell‐mediated calcium has been successfully established in a rabbit femoral artery. This model can be used to develop new devices and therapies to treat severe atherosclerotic occlusion. Copyright © 2011 John Wiley & Sons, Ltd.