Background: The implantation of a biomedical device elicits a wound-healing response that progresses through the three phases of wound healing: inflammation, cellular proliferation, and matrix remodeling. This response culminates in a fibrous collagen encapsulation of the implant. Subsequent contraction of this "scar-like" tissue can lead to physical disfigurement, implant extrusion, or impairment of implant function, necessitating surgical revision or removal. ACT1 is a synthetic peptide derived from the carboxyl-terminal sequence of the cellular gap junction protein connexin43. This novel peptide has recently been shown to modulate cutaneous wound healing, reduce scarring, and promote regenerative repair of the skin following injury. In this study, the authors investigated the ability of the ACT1 peptide to modulate the wound-healing response to biomedical device implantation.
Methods: Silicone disks coated with either vehicle control or ACT1 peptide were implanted submuscularly into male Sprague-Dawley rats. Capsulectomies were performed on days 1, 2, 3, 14, and 28. The implant capsules and surrounding tissue were analyzed histologically and biochemically.
Results: ACT1 modulated the wound-healing response to silicone implants by attenuating neutrophil infiltration, increasing vascularity of the capsule tissue, reducing type I collagen deposition around the implant, and reducing the continued presence of contractile myofibroblasts.
Conclusion: ACT1 may provide an enabling technology for modulating the wound-healing response to implants, promoting integration of implanted materials and tissue-engineered devices in the human body.