| First Author | Bjorkman KK | Year | 2020 |
| Journal | J Cell Sci | Volume | 133 |
| Issue | 15 | PubMed ID | 32620696 |
| Mgi Jnum | J:294082 | Mgi Id | MGI:6451942 |
| Doi | 10.1242/jcs.243162 | Citation | Bjorkman KK, et al. (2020) miR-206 enforces a slow muscle phenotype. J Cell Sci 133(15):jcs243162 |
| abstractText | Striated muscle is a highly specialized collection of tissues with contractile properties that vary according to functional needs. Although muscle fiber types are established postnatally, lifelong plasticity facilitates stimulus-dependent adaptation. Functional adaptation requires molecular adaptation, which is partially provided by miRNA-mediated post-transcriptional regulation. miR-206 is a muscle-specific miRNA enriched in slow muscles. We investigated whether miR-206 drives the slow muscle phenotype or is merely an outcome. We found that miR-206 expression increases in both physiological (including female sex and endurance exercise) and pathological conditions (muscular dystrophy and adrenergic agonism) that promote a slow phenotype. Consistent with that observation, the slow soleus muscle of male miR-206-knockout mice displays a faster phenotype than wild-type mice. Moreover, left ventricles of male miR-206 knockout mice have a faster myosin profile, accompanied by dilation and systolic dysfunction. Thus, miR-206 appears to be necessary to enforce a slow skeletal and cardiac muscle phenotype and to play a key role in muscle sexual dimorphisms. |
