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Skeletal muscle fibroblast collagen expression is negatively regulated by satellite cells
Author(s) -
Fry Christopher Schaffer,
Jackson Janna R,
McCarthy John J,
Peterson Charlotte A
Publication year - 2012
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.26.1_supplement.1078.15
Subject(s) - extracellular matrix , skeletal muscle , myocyte , muscle hypertrophy , microbiology and biotechnology , satellite , fibronectin , fibroblast , biology , gene expression , medicine , endocrinology , chemistry , cell culture , gene , biochemistry , genetics , engineering , aerospace engineering
Interaction between satellite cells and components of the extracellular matrix (ECM) of skeletal muscle has been demonstrated, and recent evidence suggests that satellite cells may regulate ECM remodeling following overload in muscle. We utilized mouse primary myoblasts and fibroblasts in co‐culture in addition to a genetically modified mouse model (Pax7‐DTA) to investigate the role of satellite cells in regulation of skeletal muscle ECM. The Pax7‐DTA mouse allows for the conditional ablation of >90% of satellite cells in adult mice following the administration of tamoxifen. Control/tamoxifen treated animals were randomized to sham or synergist ablation surgery, leading to overload of the plantaris muscle for 2 weeks. Microarray analysis was performed to determine if the loss of satellite cells altered plantaris gene expression. The loss of satellite cells under rest and overload conditions was associated with increased expression of a number of different collagens, as well as ECM structural and remodeling genes. Co‐culturing mouse myoblasts with fibroblasts led to a 40% decrease in the mRNA expression of Col VIa2 and Fibronectin compared to fibroblasts co‐cultured with fibroblasts. These results suggest that satellite cells are involved in the regulation and maintenance of the ECM both under rest and during muscle hypertrophy. Funding: NIAMS R01AR060701 and the Jeane B. Kempner Postdoctoral Fellowship.