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Am J Physiol Cell Physiol (August 27, 2008). doi:10.1152/ajpcell.212.2008
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Submitted on April 17, 2008
Revised on August 1, 2008
Accepted on August 21, 2008

{beta}2 integrins contribute to skeletal muscle hypertrophy in mice

Joseph S Marino1, Brian J Tausch1, Christopher L Dearth1, Marc V Manacci1, Thomas McLoughlin, PhD1, Samuel J Rakyta1, Matthew P Linsenmayer1, and Francis X. Pizza2*

1 University of Toledo
2 The University of Toledo

* To whom correspondence should be addressed. E-mail: francis.pizza{at}utoledo.edu.

We tested the contribution of {beta}2 integrins, which are important for normal function of neutrophils and macrophages, to skeletal muscle hypertrophy after mechanical loading. Using the synergist ablation model of hypertrophy and mice deficient in the common {beta} subunit of {beta}2 integrins (CD18-/-), we found that overloaded muscles of wild type mice had greater myofiber size, dry muscle mass, and total protein content compared to CD18-/- mice. The hypertrophy in wild type mice was preceded by elevations in neutrophils, macrophages, satellite cell/myoblast proliferation (BrdU+desmin+ cells), markers of muscle differentiation (MyoD1 and myogenin gene expression and formation and size of regenerating myofibers), signaling for protein synthesis (phosphorylation of Akt and p70S6k), and reduced signaling for protein degradation (decreased gene expression of MAFbx/atrogin-1). The deficiency in {beta}2 integrins however, altered the accumulation profile of neutrophils and macrophages, disrupted the temporal profile of satellite cell/myoblast proliferation, reduced markers of muscle differentiation, and impaired p70S6k signaling, all of which could serve as mechanisms for the impaired hypertrophy in overloaded CD18-/- mice. In conclusion, our findings indicate that {beta}2 integrins contribute to the hypertrophic response to muscle overload by temporally regulating satellite cells/myoblast proliferation and by enhancing muscle differentiation and p70S6k signaling.




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