Platelet-rich plasma enhances mechanical strength of strattice in rat model of ventral hernia repair.

Journal Article (Journal Article)

Incisional hernia is a common complication of hernia repair despite the development of various synthetic and bio-synthetic repair materials. Poor long-term mechanical strength, leading to high recurrence rates, has limited the use of acellular dermal matrices (ADMs) in ventral hernia repair (VHR). Biologically derived meshes have been an area of increasing interest. Still these materials bring the risk of more aggressive immune response and fibrosis in addition to the mechanical failures suffered by the synthetic materials. Platelet-rich plasma (PRP), a growth-factor-rich autologous blood product, has been shown to improve early neovascularization, tissue deposition, and to decrease the rates of recurrence. Here, we demonstrate that PRP promotes the release of growth factors stromal derived factor (SDF)-1, transforming growth factor-beta, and platelet-derived growth factor in a dose-dependent manner. Additionally, we utilize an aortic ring angiogenesis assay to show that PRP promotes angiogenesis in vitro. A rat model of VHR using StratticeTM ADM demonstrates similar findings in vivo, corresponding with the increased expression of vascular endothelial growth factor and collagen type 1 alpha 1. Finally, we show that the molecular and cellular activity initiated by PRP results in an increased mechanical stiffness of the hernia repair mesh over time. Collectively, these data represent an essential step in demonstrating the utility and the mechanism of platelet-derived plasma in biomaterial-aided wound healing and provide promising preclinical data that suggest such materials may improve surgical outcomes.

Full Text

Duke Authors

Cited Authors

  • Fernandez-Moure, JS; Van Eps, JL; Scherba, JC; Yazdi, IK; Robbins, A; Cabrera, F; Vatsaas, C; Moreno, M; Weiner, BK; Tasciotti, E

Published Date

  • July 2021

Published In

Volume / Issue

  • 15 / 7

Start / End Page

  • 634 - 647

PubMed ID

  • 33880858

Electronic International Standard Serial Number (EISSN)

  • 1932-7005

Digital Object Identifier (DOI)

  • 10.1002/term.3200

Language

  • eng

Conference Location

  • England