Local tissue geometry determines contractile force generation of engineered muscle networks.

Published

Journal Article

The field of skeletal muscle tissue engineering is currently hampered by the lack of methods to form large muscle constructs composed of dense, aligned, and mature myofibers and limited understanding of structure-function relationships in developing muscle tissues. In our previous studies, engineered muscle sheets with elliptical pores ("muscle networks") were fabricated by casting cells and fibrin gel inside elastomeric tissue molds with staggered hexagonal posts. In these networks, alignment of cells around the elliptical pores followed the local distribution of tissue strains that were generated by cell-mediated compaction of fibrin gel against the hexagonal posts. The goal of this study was to assess how systematic variations in pore elongation affect the morphology and contractile function of muscle networks. We found that in muscle networks with more elongated pores the force production of individual myofibers was not altered, but the myofiber alignment and efficiency of myofiber formation were significantly increased yielding an increase in the total contractile force despite a decrease in the total tissue volume. Beyond a certain pore length, increase in generated contractile force was mainly contributed by more efficient myofiber formation rather than enhanced myofiber alignment. Collectively, these studies show that changes in local tissue geometry can exert both direct structural and indirect myogenic effects on the functional output of engineered muscle. Different hydrogel formulations and pore geometries will be explored in the future to further augment contractile function of engineered muscle networks and promote their use for basic structure-function studies in vitro and, eventually, for efficient muscle repair in vivo.

Full Text

Duke Authors

Cited Authors

  • Bian, W; Juhas, M; Pfeiler, TW; Bursac, N

Published Date

  • May 2012

Published In

Volume / Issue

  • 18 / 9-10

Start / End Page

  • 957 - 967

PubMed ID

  • 22115339

Pubmed Central ID

  • 22115339

Electronic International Standard Serial Number (EISSN)

  • 1937-335X

International Standard Serial Number (ISSN)

  • 1937-3341

Digital Object Identifier (DOI)

  • 10.1089/ten.tea.2011.0313

Language

  • eng