Abstract
The aim of this study was to investigate the molecular mechanisms underlying the problem of infection and pro-fibrotic tissue rearrangement around artificial devices used for soft tissue augmentation. An allogenous, acellularized dermal matrix (aADM) was implanted into subcutaneous pockets at the groin in 10 male Wistar rats. After 7 or 14 days, tissue specimens were obtained and analyzed for transforming growth factor (TGF)-beta1 and vascular endothelial growth factor (VEGF) by immunoblotting as well as alpha-smooth muscle actin (SMA)-and endoglin (CD105)-expression by immunohistochemistry. A TGFbeta1-dependent alpha-SMA-overexpression as well as capillary lumina area regression were observed in the peri-implant connective tissue. VEGF expression decreased over the entire investigation period and resulted in delayed neovascularization of the implant. In conclusion, these experiments demonstrate that co-delivery of anti-fibrotic and pro-angiogenic agents is highly desirable to improve the clinical success of artificial tissue substitutes.
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