Diminished satellite cells and elevated adipogenic gene expression in muscle as caused by ovariectomy are averted by low-magnitude mechanical signals.
Age-related degeneration of the musculoskeletal system, accelerated by menopause, is further complicated by increased systemic and muscular adiposity. The purpose of this study was to identify at the molecular, cellular, and tissue levels the impact of ovariectomy on adiposity and satellite cell populations in mice and whether mechanical signals could influence any outcomes. Eight-week-old C57BL/6 mice were ovariectomized, with one half subjected to low-intensity vibration (LIV; 0.3 g/90 Hz, 15 min/day, 5 day/wk; n = 10) for 6 wk and the others sham vibrated (OVX; n = 10). Data are compared with age-matched, intact controls (AC; n = 10). In vivo μCT analysis showed that OVX mice gained 43% total (P < 0.001) and 125% visceral adiposity (P < 0.001) compared with their baseline after 6 wk, whereas LIV gained only 21% total (P = 0.01) and 70% visceral adiposity (P < 0.01). Relative to AC, expression of adipogenic genes (PPARγ, FABP4, PPARδ, and FoxO1) was upregulated in OVX muscle (P < 0.05), whereas LIV reduced these levels (P < 0.05). Adipogenic gene expression was inversely related to the percentage of total and reserve satellite cell populations in the muscle, with both declining in OVX compared with AC (-21 and -28%, respectively, P < 0.01). LIV mitigated these declines (-11 and -17%, respectively). These results provide further evidence of the negative consequences of estrogen depletion and demonstrate that mechanical signals have the potential to interrupt subsequent adipogenic gene expression and satellite cell suppression, emphasizing the importance of physical signals in protecting musculoskeletal integrity and slowing the fat phenotype.
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY.
Danielle M
http://orcid.org/0000-0003-2636-2993
DM
Frechette
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY.
Divya
D
Krishnamoorthy
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY.
Benjamin J
BJ
Adler
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY.
M Ete
ME
Chan
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY clinton.rubin@stonybrook.edu.
Clinton T
CT
Rubin
D050156:Adipogenesis / Q000235:genetics*; D054392:Adipokines / Q000096:biosynthesis / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight; D004435:Eating; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010052:Ovariectomy; D010812:Physical Stimulation; D032496:Satellite Cells, Skeletal Muscle / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D014057:Tomography, X-Ray Computed; D015854:Up-Regulation; D014732:Vibration
D054392:Adipokines; D015415:Biomarkers
muscle stem cells; myogenesis; skeletal muscle; vibration