| First Author | Jackson MF | Year | 2014 |
| Journal | Endocrinology | Volume | 155 |
| Issue | 5 | Pages | 1771-85 |
| PubMed ID | 24517228 | Mgi Jnum | J:210483 |
| Mgi Id | MGI:5571243 | Doi | 10.1210/en.2013-2014 |
| Citation | Jackson MF, et al. (2014) Myostatin regulates tissue potency and cardiac calcium-handling proteins. Endocrinology 155(5):1771-85 |
| abstractText | Attenuating myostatin enhances striated muscle growth, reduces adiposity, and improves cardiac contractility. To determine whether myostatin influences tissue potency in a manner that could control such pleiotropic actions, we generated label-retaining mice with wild-type and mstn(-/-) (Jekyll) backgrounds in which slow-cycling stem, transit-amplifying, and progenitor cells are preferentially labeled by histone 2B/green fluorescent protein. Jekyll mice were born with fewer label-retaining cells (LRCs) in muscle and heart, consistent with increased stem/progenitor cell contributions to embryonic growth of both tissues. Cardiac LRC recruitment from noncardiac sources occurred in both groups, but lasted longer in Jekyll hearts, whereas heightened beta-adrenergic sensitivity of mstn(-/-) hearts was explained by elevated SERCA2a, phospholamban, and beta2-adrenergic receptor levels. Jekyll mice were also born with more adipose LRCs despite significantly smaller tissue weights. Reduced adiposity in mstn(-/-) animals is therefore due to reduced lipid deposition as adipoprogenitor pools appear to be enhanced. By contrast, increased bone densities of mstn(-/-) mice are likely compensatory to hypermuscularity because LRC counts were similar in Jekyll and wild-type tibia. Myostatin therefore significantly influences the potency of different tissues, not just muscle, as well as cardiac Ca(2)(+)-handling proteins. Thus, the pleiotropic phenotype of mstn(-/-) animals may not be due to enhanced muscle development per se, but also to altered stem/progenitor cell pools that ultimately influence tissue potency. |
