Abstract 14609: Fibronectin Surface Coating Accelerates the Autologous in vivo Recellularization of Decellularized Aortic Conduits in a Rat Implantation Model
Objectives Decellularization is a promising option to diminish immune and inflammatory response against cardiovascular implants. In order to accelerate the autologous in vivo recellularization of aortic conduits, which is crucial for their biocompatibility, we tested fibronectin surface coating in a standardized rat implantation model.
Methods Detergent-decellularized rat aortic conduits (n=36) were surface coated with covalently Alexa488-labelled fibronectin (FN; 50 µg/ml, 24 hours) and implanted into the systemic circulation of Wistar rats (groupA; n=18). Uncoated implants served as controls (groupB; n=18). At days 0, 1, 7, 28 and 56, fluorescence-based detection of FN coating was conducted. Cellular repopulation was examined by histology and immunohistology. RNA analysis after explantation was performed by quantitative realtime PCR.
Results All rats survived the study without clinical or sonographic lower body malperfusion. FN-bound fluorescence on both surfaces of the aortic conduits was bright at days 0 and 1 and decreased after 1 week, though, it was still present after 4 and 8 weeks. Luminal endothelialization was accelerated in the FN group (p>0.01), however, local myofibroblast hyperplasia with increased ratio of intima-to-media thickness occurred. Originating from the adventitial surface, alpha-smooth muscle actin positive cell invasion into the media of FN-coated conduits was significantly increased compared to control animals (p>0.01). In these medial areas, in situ zymography revealed increased matrix metalloproteinase acticity. In both groups, inflammatory cell markers (CD3 & CD68) proved negative.
Conclusions FN surface coating of decellularized cardiovascular implants proved feasible and persistent for at least 8 weeks in the systemic circulation. Biofunctional protein coating accelerated the autologous in vivo reendothelialization and induced a significantly increased medial recellularization.
- © 2012 by American Heart Association, Inc.