RESUMEN
Organ decellularization is one of the most promising approaches of tissue engineering to overcome the shortage of organs available for transplantation. However, there are key hurdles that still hinder its clinical application, and the lack of hemocompatibility of decellularized materials is a central one. In this work, we demonstrate that Custodiol (HTK solution), a common solution used in organ transplantation, increased the hemocompatibility of acellular scaffolds obtained from rat livers. We showed that Custodiol inhibited ex vivo, in vitro, and in vivo blood coagulation to such extent that allowed successful transplantation of whole-liver scaffolds into recipient animals. Scaffolds previously perfused with Custodiol showed no signs of platelet aggregation and maintained in vitro and in vivo cellular compatibility. Proteomic analysis revealed that proteins related to platelet aggregation were reduced in Custodiol samples while control samples were enriched with thrombogenicity-related proteins. We also identified distinct components that could potentially be involved with this anti-thrombogenic effect and thus require further investigation. Therefore, Custodiol perfusion emerge as a promising strategy to reduce the thrombogenicity of decellularized biomaterials and could benefit several applications of whole-organ tissue engineering.