Histology revealed an intracellular organization resembling that of native muscle.
Existing in vitro models of human skeletal muscle cannot recapitulate the organization and function of native muscle, limiting their use in physiological and pharmacological studies.
Expansion of primary human myoblasts and formation of myotubes in two-dimensional (2D) systems is well known, however, these cultures are difficult to maintain over long times, lack the architecture of native muscle, and require complex media components to initiate spontaneous contractions (Blau and Webster, 1981; Eberli et al., 2009; Guo et al., 2014).
The ATP sensitivity of the native muscle KATP channel was significantly reduced compared with control mice (Fig. 2a-d).
In the only work measuring omega currents in human muscle fibres (Jurkat-Rott et al. 2009), which are always heterozygous because of the autosomal dominant inheritance of the disease, R528H native muscle fibres had a conductance of 12 µS/cm, which is indeed about half of the conductance of the homozygous R528H mouse muscle fibres of 28 µS/cm.
Myoblast-seeded scaffolds enabled remarkable muscle regeneration with high myofiber and vascular densities after 2 and 4 weeks, mimicking that of native skeletal muscle, while acellular scaffolds lacked muscle regeneration.
In the present report, we present evidence that a similar posttranslational modification of the native muscle-type PFK1 may also occur in mammalian cancer cells that consequently leads to the formation of active shorter PFK1 fragments with changed kinetic parameters.
To further optimize muscle engineered constructs, we have developed a novel bioreactor system (MagneTissue) for rapid engineering of skeletal muscle-like constructs with the aim to resemble native muscle in terms of structure, gene expression profile and maturity.
In response to an anti-malarial agent, chloroquine, myobundles showed induction of autophagic myopathy also observed in native muscle (Shintani and Klionsky, 2004), thus providing a potential functional screen for non-toxic modulators of autophagy.
Specifically, we eliminated the mentioning of disease from the following sentences: In the Discussion: "In response to an anti-malarial agent, chloroquine, myobundles showed induction of autophagic myopathy also observed in native muscle (Shintani and Klionsky, 2004), thus providing a potential functional screen for non-toxic modulators of autophaghy".
Since engineered muscle, unlike most native muscle tissue, is composed of relatively short myofibers, we hypothesized that, its force production and transmission would be profoundly influenced by cell-matrix interactions.
