title: The connexin43 carboxyl-terminal peptide ACT1 modulates the biological response to silicone implants.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Columbia and Charleston, S.C. From the Department of Surgery, Division of Plastic Surgery, and Department of Cell and Developmental Biology and Anatomy, University of South Carolina School of Medicine, and the Department of Cell Biology and Anatomy, Center for Cardiovascular Developmental Biology, Department of Pediatric Cardiology, Joint Clemson University-MUSC Bioengineering Program, and Cardiovascular Developmental Biology Center, Medical University of South Carolina.
authors.forename: Brent L
authors.initials: BL
authors.lastname: Soder
authors.forename: John T
authors.initials: JT
authors.lastname: Propst
authors.forename: Timothy M
authors.initials: TM
authors.lastname: Brooks
authors.forename: Richard L
authors.initials: RL
authors.lastname: Goodwin
authors.forename: Harold I
authors.initials: HI
authors.lastname: Friedman
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Yost
authors.forename: Robert G
authors.initials: RG
authors.lastname: Gourdie
mesh_terms: D000818:Animals; D001672:Biocompatible Materials / Q000009:adverse effects*; D018427:Breast Implants / Q000009:adverse effects*; D018031:Connexin 43 / Q000008:administration & dosage*; D017630:Connexins; D004195:Disease Models, Animal; D007155:Immunologic Factors / Q000008:administration & dosage*; D008297:Male; D010446:Peptide Fragments / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012828:Silicones / Q000009:adverse effects*; D014945:Wound Healing / Q000187:drug effects*
chemical_list: C541130:ACT1 protein; D001672:Biocompatible Materials; D018031:Connexin 43; D017630:Connexins; D007155:Immunologic Factors; D010446:Peptide Fragments; D012828:Silicones