Decellularised skeletal muscles allow functional muscle regeneration by promoting host cell migration

Urciuolo, A., Urbani, L., Perin, S., Maghsoudlou, P., Scottoni, F., Gjinovci, A., Collins-Hooper, H., Loukogeorgakis, S., Tyrakis, A., Torelli, S., Germinario, E., Fallas, M., Julia-Vilella, C., Eaton, S., Blaauw, B., Patel, K. and De Coppi, P. (2018) Decellularised skeletal muscles allow functional muscle regeneration by promoting host cell migration. Scientific Reports, 8. 8398. ISSN 2045-2322 doi: 10.1038/s41598-018-26371-y

Abstract/Summary

Pathological conditions affecting skeletal muscle function may lead to irreversible volumetric muscle loss (VML). Therapeutic approaches involving acellular matrices represent an emerging and promising strategy to promote regeneration of skeletal muscle following injury. Here we investigated the ability of three different decellularised skeletal muscle scaffolds to support muscle regeneration in a xenogeneic immune-competent model of VML, in which the EDL muscle was surgically resected. All implanted acellular matrices, used to replace the resected muscles, were able to generate functional artificial muscles by promoting host myogenic cell migration and differentiation, as well as nervous fibres, vascular networks, and satellite cell (SC) homing. However, acellular tissue mainly composed of extracellular matrix (ECM) allowed better myofibre three-dimensional (3D) organization and the restoration of SC pool, when compared to scaffolds which also preserved muscular cytoskeletal structures. Finally, we showed that fibroblasts are indispensable to promote efficient migration and myogenesis by muscle stem cells across the scaffolds in vitro. This data strongly support the use of xenogeneic acellular muscles as device to treat VML conditions in absence of donor cell implementation, as well as in vitro model for studying cell interplay during myogenesis.

Item Type	Article
URI	https://reading-clone.eprints-hosting.org/id/eprint/76798
Identification Number/DOI	10.1038/s41598-018-26371-y
Refereed	Yes
Divisions	Life Sciences > School of Biological Sciences > Biomedical Sciences
Publisher	Nature Publishing Group
Download/View statistics	View download statistics for this item