After this breakthrough, the X-ray crystallographic structures of mouse muscle-type α1 (Dellisanti et al., 2007), two α7 nAChR ECD-AChBPs chimeras (Li et al., 2011; Nemecz and Taylor, 2011), human neuronal α9 nAChR ECD (Zouridakis et al., 2014), and the full-length heteromeric human (α4 3 β2)2 receptor were determined in quick succession (Morales-Perez et al., 2016).
9 Furthermore, it has been shown that overexpression of Nogo-A in wild-type mouse muscle affects the NMJ with fragmentation of the postsynaptic compartment and loss of nerve muscle contact.
This raises the question of whether one type of mouse muscle more accurately represents particular (myopathic) characteristics in a given human muscle type than another.
We compared expression patterns of genes that are differentially expressed between muscle types in mice fed a low fat diet (LFD) with mice fed an HFD.
Employing AAV6 vector dosages typically used in preclinical gene transfer studies (3×1010 –1 × 1011 particles), we found that hrGFP caused dose-dependent myopathy when delivered to wild-type (wt) mouse muscle, whereas identical titers of AAV6 carrying eGFP were relatively benign.
We also extended these studies to differentiated primary mouse muscle cell cultures; we observed two types of myotubes in primary cultures: thin slowly contracting myotubes with nuclei aligned along the middle of the fiber (immature myotubes), and thicker, faster contracting myotubes often with small or large nuclei clusters (mature myotubes).
The mdx soleus, a mouse muscle more representative of human fiber type composition, demonstrated the most profound improvement in force production and a shift toward faster myosin-heavy chain isoforms.
Mouse and human skeletal muscle transcriptome profiles vary by muscle type, raising the question of which mouse muscle groups have the greatest molecular similarities to human skeletal muscle.
NMJs in all three muscle types from Rab18 −/− mice showed distinctive large accumulations at both stages, progressing from 30% of terminals in early symptomatic muscles to 60% by mid-late-symptomatic timepoints in FDB and lumbrical muscles (Fig. 4J K).
Some studies have shown, however, that resistance training in humans can also cause shifts in fiber type not seen in these mouse models of postnatal muscle hypertrophy, and mouse muscle contains relatively more fast fibers than human muscle [43].
