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Early time course of Pax3, Pax7, and MyoD protein content in the functionally overloaded rat plantaris muscle
Author(s) -
Kander Elizabeth M.,
McCall Gary E.,
Zhong Hui,
Roy Roland R.,
Hyatt JonPhilippe K.
Publication year - 2007
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.21.6.a945-a
Subject(s) - myod , myod protein , pax3 , myogenin , myogenic regulatory factors , skeletal muscle , myocyte , biology , medicine , endocrinology , muscle hypertrophy , microbiology and biotechnology , myogenesis , transcription factor , genetics , gene
Recent evidence implicates Pax3 and Pax7 as upstream transcriptional regulators of muscle regulatory factors (e.g., MyoD) in skeletal muscle. Pax3 and Pax7 are thought to direct muscle precursor (satellite) cell proliferation and self‐renewal and also commit adult stem cells (non‐satellite cells) into a myogenic lineage. We functionally overloaded (FO) the plantaris muscle in adult rats via surgical ablation of the gastrocnemius muscle and then assessed whole‐muscle Pax3, Pax7, and MyoD protein content after 12h, 1, 2, 3, and 7 days using western blot analysis. Relative to control rats, FO muscle mass increased ~7 and 12% on day 3 and 7 , respectively (P< 0.05). Pax3, Pax7, and MyoD expression rose at 12h and 1 day (P> 0.05) and peaked on days 2 and 3 (P< 0.05). Day 2 expression for Pax3, Pax7, and MyoD were ~4‐, 4‐, and 2‐fold higher in FO than control rats, respectively. Day 3 expression for Pax3, Pax7, and MyoD expression were ~7‐, ~6‐, and ~2‐fold higher in FO than control rats, respectively, and returned to baseline by day 7 . These results indicate that Pax3 and Pax7 proteins follow a similar temporal pattern of expression as a muscle regulatory factor (MyoD) known to be important for muscle hypertrophy. Our next objective is to discriminate whether satellite cells or adult stem cells are the principal source of Pax3 and Pax7 expression in hypertrophying skeletal muscle. Funded in part by NIH NS16333