Soder Brent L, Propst John T, Brooks Timothy M, Goodwin Richard L, Friedman Harold I, Yost Michael J, Gourdie Robert G
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.
Plast Reconstr Surg. 2009 May;123(5):1440-1451. doi: 10.1097/PRS.0b013e3181a0741d.
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.
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.
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.
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.
生物医学装置的植入会引发伤口愈合反应，该反应会经历伤口愈合的三个阶段：炎症、细胞增殖和基质重塑。这种反应最终会导致植入物被纤维性胶原蛋白包裹。随后这种“瘢痕样”组织的收缩会导致身体变形、植入物挤出或植入物功能受损，从而需要进行手术修复或移除。ACT1是一种源自细胞间隙连接蛋白连接蛋白43羧基末端序列的合成肽。最近已证明这种新型肽可调节皮肤伤口愈合、减少瘢痕形成并促进损伤后皮肤的再生修复。在本研究中，作者研究了ACT1肽调节对生物医学装置植入的伤口愈合反应的能力。
将涂有载体对照或ACT1肽的硅胶盘植入雄性Sprague-Dawley大鼠的肌肉下。在第1、2、3、14和28天进行包膜切除术。对植入物包膜和周围组织进行组织学和生化分析。
ACT1通过减弱中性粒细胞浸润、增加包膜组织的血管形成、减少植入物周围I型胶原蛋白沉积以及减少收缩性肌成纤维细胞的持续存在来调节对硅胶植入物的伤口愈合反应。
ACT1可能为调节对植入物的伤口愈合反应提供一种使能技术，促进植入材料和组织工程装置在人体中的整合。
