Journal
JOURNAL OF CELL SCIENCE
Volume 133, Issue 15, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.243162
Keywords
miR-206; miRNA; Skeletal muscle; Heart; Sexual dimorphism
Categories
Funding
- National Institutes of Health [GM29090, 2T32HL007822-11A2, 5T32GM007135-36, K01AR055676]
- American Heart Association [13POST14410014]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available