RESUMEN
The imbalance between endogenous and exogenous healing is the fundamental reason for the poor tendon healing. In this study, a Janus patch was developed to promote endogenous healing and inhibit exogenous healing, leading to improved tendon repair. The upper layer of the patch is a poly(dl-lactide-co-glycolide)/polycaprolactone (PLGA/PCL) nanomembrane (PMCP-NM) modified with poly(2-methylacryloxyethyl phosphocholine) (PMPC), which created a lubricated and antifouling surface, preventing cell invasion and mechanical activation. The lower layer is a PLGA/PCL fiber membrane loaded with fibrin (Fb) (Fb-NM), serving as a temporary chemotactic scaffold to regulate the regenerative microenvironment. In vitro, the Janus patch effectively reduced 92.41% cell adhesion and 79.89% motion friction. In vivo, the patch inhibited tendon adhesion through the TGF-ß/Smad signaling pathway and promoted tendon maturation. This Janus patch is expected to provide a practical basis and theoretical guidance for high-quality soft tissue repair.
Asunto(s)
Tendones , Cicatrización de Heridas , Tendones/fisiología , Adhesión CelularRESUMEN
Due to the limitations of tendon biology, high-quality tendon repair remains a clinical and scientific challenge. Here, a micro-nano hierarchical scaffold is developed to promote orderly tendon regeneration by providing temporal-matched biological constraints. In short, fibrin (Fb), which provides biological constraints, is loaded into poly (DL-lactide-co-glycolide) nanoyarns with suitable degradation cycles (Fb-loaded nanofiber yarns (Fb-NY)). Then further combined with braiding technology, temporary chemotactic Fb scaffolds with tendon extracellular matrix-like structures are obtained to initiate the regeneration process. At the early stage of healing (2 w), the regeneration microenvironment is regulated (inducing M2 macrophages and restoring the early blood supply necessary for healing) by Fb, and the alignment of cells and collagen is induced by nanoyarn. At the late healing stage (8 w), with the degradation of Fb-NY, non-functional vascular regression occurs, and the newborn tissues gradually undergo load-bearing remodeling, restoring the anvascularous and ordered structure of the tendon. In summary, the proposed repair strategy provides temporal-matched biological constraints, offering a potential pathway to reconstruct the ordered structure and function of tendons.