Abstract
Decellularization of non-autologous biological implants reduces the immune response against foreign tissue. Striving for in vivo repopulation of aortic prostheses with autologous cells, thereby improving the graft biocompatibility, we examined surface coating with laminin in a standardized rat implantation model. Detergent-decellularized aortic grafts from donor rats (n = 37) were coated with laminin and systemically implanted into Wistar rats. Uncoated implants served as controls. Implant re-colonization and remodeling were examined by scanning electron microscopy (n = 10), histology and immunohistology (n = 18). Laminin coating persisted over eight weeks. Two weeks after implantation, no relevant neoendothelium formation was observed, whereas it was covering the whole grafts after eight weeks, with a significant acceleration in the laminin group (p = 0.0048). Remarkably, the intima-to-media ratio, indicating adverse hyperplasia, was significantly diminished in the laminin group (p = 0.0149). No intergroup difference was detected in terms of medial recellularization (p = 0.2577). Alpha-smooth muscle actin-positive cells originating from the adventitial surface invaded the media in both groups to a similar extent. The amount of calcifying hydroxyapatite deposition in the intima and the media did not differ between the groups. Inflammatory cell markers (CD3 and CD68) proved negative in coated as well as uncoated decellularized implants. The coating of decellularized aortic implants with bioactive laminin caused an acceleration of the autologous recellularization and a reduction of the intima hyperplasia. Thereby, laminin coating seems to be a promising strategy to enhance the biocompatibility of tissue-engineered vascular implants.
Highlights
Cardiovascular disease is the main cause of death globally [1]
Decellularization reduces the inflammatory response against non-autologous implants [5]
Implant coating with bioactive proteins can further accelerate the repopulation process [7,8,9]
Summary
Cardiovascular disease is the main cause of death globally [1]. In case of need for small-caliber arterial replacement, artificial implants have proven to be insufficient, and autologous grafts are frequently limited in terms of wall quality, availability, and long-term durability. in the last decade, tissue-engineered large-caliber arterial and valvular grafts have presented good patency and mid-term durability in preclinical animal models as well as in humans [2,3,4].For small-caliber arterial grafts, decellularization has been shown to improve their performance in smallMaterials 2019, 12, 3351; doi:10.3390/ma12203351 www.mdpi.com/journal/materialsMaterials 2019, 12, 3351 animal models as well. In case of need for small-caliber arterial replacement, artificial implants have proven to be insufficient, and autologous grafts are frequently limited in terms of wall quality, availability, and long-term durability. In the last decade, tissue-engineered large-caliber arterial and valvular grafts have presented good patency and mid-term durability in preclinical animal models as well as in humans [2,3,4]. For small-caliber arterial grafts, decellularization has been shown to improve their performance in small. Decellularization reduces the inflammatory response against non-autologous implants [5]. Implant coating with bioactive proteins can further accelerate the repopulation process [7,8,9]. Beneficial results, such as rapid re-endothelialization and cell migration into the media without any inflammatory reactions, were observed in coated grafts, and adverse intima hyperplasia occurred [7,8]
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