By a News Reporter-Staff News Editor at Angiogenesis Weekly -- Fresh data on Biomedicine and Biomedical Engineering are presented in a new report. According to news reporting originating from Seattle, Washington, by NewsRx correspondents, research stated, "Survival of tissue engineered constructs after implantation depends heavily on induction of a vascular response in host tissue, promoting a quick anastomosis of the cellular graft. Additionally, implanted constructs typically induce fibrous capsule formation, effectively preventing graft integration with host tissue."
Our news editors obtained a quote from the research from the University of Washington, "Previously we described the development of a high density microtemplated fibrin scaffold for cardiac tissue engineering applications with tunable degradation and mechanical properties which promoted seeded cell survival and organization in vitro (Thomson et al., Tissue Eng Part A, 2013). Scaffold degradation in vitro was controllable by addition of the serine protease inhibitor aprotinin and/or the fibrin cross-linker Factor XIII (FXIII). The goal of this study was to assess host tissue responses to these fibrin scaffold formulations by determining effects on scaffold degradation, angiogenic responses, and fibrous capsule formation in a subcutaneous implant model. Aprotinin significantly decreased scaffold degradation over 2 weeks of implantation. A significant increase in capillary infiltration of aprotinin implants was found after 1 and 2 weeks, with a significantly greater amount of capillaries reaching the interior of aprotinin scaffolds. Interestingly, after 2 weeks the aprotinin scaffolds had a significantly thinner, yet apparently more cellular fibrous capsule than unmodified scaffolds. These results indicate aprotinin not only inhibits fibrin scaffold degradation, but also induces significant responses in the host tissue. These included an angiogenic response resulting in increased vascularization of the scaffold material over a relatively short period of time."
According to the news editors, the research concluded: "In addition, aprotinin release from scaffolds may reduce fibrous capsule formation, which could help promote improved integration of cell-seeded scaffolds with host tissue."
For more information on this research see: Proangiogenic microtemplated fibrin scaffolds containing aprotinin promote improved wound healing responses. Angiogenesis, 2014;17(1):195-205. Angiogenesis can be contacted at: Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands. (Springer - www.springer.com; Angiogenesis - www.springerlink.com/content/0969-6970/)
The news editors report that additional information may be obtained by contacting K.S. Thomson, University of Washington, Dept. of Med Cardiol, Seattle, WA 98109, United States. Additional authors for this research include S.K. Dupras, C.E. Murry, M. Scatena and M. Regnier (see also Biomedicine and Biomedical Engineering).
Keywords for this news article include: Tissue Engineering, Biomedicine and Biomedical Engineering, Seattle, Washington, United States, Bioengineering, North and Central America
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