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J Physiol Volume 570, Number 1, 157-167, January 1, 2006 DOI: 10.1113/jphysiol.2005.093005
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Stress-dependent and -independent expression of the myogenic regulatory factors and the MARP genes after eccentric contractions in rats

Eric R. Hentzen1, Michele Lahey1, David Peters1, Liby Mathew1, Ilona A. Barash1, Jan Fridén2 and Richard L. Lieber1

1 Departments of Orthopaedic Surgery and Bioengineering, and the Biomedical Sciences Graduate Group, University of California and Veterans Administration Medical Centers, San Diego, CA, USA
2 Department of Hand Surgery, Sahlgrenska University Hospital, Göteborg, Sweden

Abstract

The relationship between muscle mechanical conditions and gene expression was investigated by varying both stress and contraction mode imposed upon rat dorsiflexors (n= 25), activating them at high or low frequencies (150 Hz or 40 Hz) either eccentrically or isometrically. Muscle physiological, immunohistochemical and gene expression changes were then measured 24 h after the exercise bout. Peak stress was the best predictor of muscle injury, independent of contraction mode (i.e. eccentric or isometric). When peak stresses were matched, no physiological or immunohistochemical differences were detected between isometric and eccentric contractions. The expression of certain myogenic regulatory and muscle ankyrin repeat protein (MARP) genes (myoD, myogenin, MLP and CARP) depended both on peak muscle stress achieved during contraction and contraction mode. In contrast, Arpp/Ankrd2 was dramatically upregulated only by eccentric contractions, but not by isometric contractions, even though the stress level of the eccentric contractions varied over a three-fold range and overlapped with that of the isometric group. The role that Arpp/Ankrd2 upregulation plays in the biological response to eccentric contraction remains to be determined, as does the control mechanism whereby the expression of certain genes (such as myoD, myogenin, MLP and CARP) is sensitive to muscle stress while another (Arpp/Ankrd2) is sensitive only to contraction mode.

(Received 20 September 2005; accepted after revision 20 October 2005; first published online 20 October 2005)
Corresponding author R. L. Lieber: Department of Orthopaedics (9151), V.A. Medical Center and UC San Diego, 3350 La Jolla Village Drive, San Diego, CA 92161, USA. Email: rlieber{at}ucsd.edu




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Errata
J. Physiol., January 15, 2006; 570(2): 429 - 429.
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