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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 102/4/1640    most recent 01397.2006v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Esposito, A. Articles by Danieli-Betto, D. Search for Related Content PubMed PubMed Citation Articles by Esposito, A. Articles by Danieli-Betto, D.

Isoform switching in myofibrillar and excitation-contraction coupling proteins contributes to diminished contractile function in regenerating rat soleus muscle

¹Department of Human Anatomy and Physiology, University of Padova, Padova, Italy; ²Istituto Interuniversitario di Miologia, Padova, Italy; ³Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and ⁴Muscle Biology and Physiopathology Unit, Consiglio Nazionale delle Ricerche Neuroscience Institute, Padova, Italy

Submitted 11 December 2006 ; accepted in final form 10 January 2007

Postnatal development of skeletal muscle occurs through the progressive transformation of diverse biochemical, metabolic, morphological, and functional characteristics from the embryonic to the adult phenotype. Since muscle regeneration recapitulates postnatal development of muscle fiber, it offers an appropriate experimental model to investigate the existing relationships between diverse muscle functions and the expression of key protein isoforms, particularly at the single-fiber level. This study was carried out in regenerating soleus muscle 14 days after injury. At this intermediate stage, the regenerating muscle exhibited a recovery of mass greater than its force generation capacity. The lower specific tension of regenerating muscle suggested intrinsic defective excitation-contraction coupling and/or contractility processes. The presence of developmental isoforms of both the voltage-gated Ca²⁺ channel (₁C) and of ryanodine receptor 3, paralleled by an abnormal caffeine contracture development, confirms the immature excitation-contraction coupling of the regenerating muscle. The defective Ca²⁺ handling could also be confirmed by the lower sarcoplasmic reticulum caffeine sensitivity of regenerating single fibers. Also, regenerating single fibers revealed a lower maximal specific tension, which was associated with the residual presence of embryonic myosin heavy chains. Moreover, the fibers showed a reduced Ca²⁺ sensitivity of myofibrillar proteins, particularly those simultaneously expressing the slow and fast isoforms of troponin C. The present results indicate that the expression of developmental proteins determines the incomplete functional recovery of regenerating soleus.

pCa-tension relationship; troponin C; myosin heavy chains; sarcoplasmic reticulum caffeine sensitivity; ryanodine and dihydropyridine receptors