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Sphingomyelinase promotes atrophy in C2C12 myotubes
Author(s) -
Schwagerl Peter Jerome,
Talbert Erin E.,
Nguyen Linda M.D.,
Powers Scott K.,
Ferreira Leonardo F.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb602
Subject(s) - myogenesis , c2c12 , skeletal muscle , muscle atrophy , atrophy , sphingomyelin , myocyte , medicine , endocrinology , biology , chemistry , anatomy , cholesterol
Chronic heart failure, sepsis, and cancer chemotherapy lead to skeletal muscle atrophy. In all these conditions, the activity of sphingomyelinase (SMase) in the plasma is elevated. SMase has been shown to activate proteolytic pathways in non‐muscle cells. We tested the hypothesis that exogenous SMase promotes atrophy in skeletal muscle cells. Differentiated C2C12 myotubes were exposed to SMase (0.5 U/ml) or vehicle every 24 hrs for 48 hrs. We used brightfield microscopy to acquire images for measurement of myotube width (3 images per well). All myotubes within each field of view were analyzed (total: SMase 112 and vehicle 101 myotubes). Myotube widths were compiled to provide an average per well (n = 3/group). Initial analysis showed that SMase decreased myotube width by ~25% (mean±SD; vehicle 25.3±2.4 μm, SMase 18.9±1.2 μm; P < 0.05). Our data suggests that SMase promotes skeletal muscle atrophy. This is consistent with activation of proteolytic pathways. Funding support: NIH/NHLBI 1K99HL098453‐01