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Slowed relaxation and preserved maximal force in soleus muscles of mice with targeted disruption of the Serca2 gene in skeletal muscle
Author(s) -
Sjåland Cecilie,
Lunde Per Kristian,
Swift Fredrik,
Munkvik Morten,
Ericsson Madelene,
Lunde Marianne,
Boye Sigurd,
Christensen Geir,
Ellingsen Øyvind,
Sejersted Ole M.,
Andersson Kristin B.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.211987
Subject(s) - soleus muscle , skeletal muscle , anatomy , chemistry , biology
Non‐technical summary Muscle function depends on tightly regulated Ca 2+ movement between the intracellular sarcoplasmic reticulum (SR) Ca 2+ store and cytoplasm in muscle cells. Disturbances in these processes have been linked to impaired muscle function and muscle disease. We disrupted the gene for the SERCA2 SR Ca 2+ pump in mouse skeletal muscle to study how decreased transport of Ca 2+ into the SR would affect soleus muscle function. We found that the SERCA2 content was strongly reduced in the 40% fraction of soleus muscle fibres normally expressing SERCA2. Muscle relaxation was slowed, supporting the hypothesis that reduced SERCA2 would reduce Ca 2+ transport into the SR and prolong muscle relaxation time. Surprisingly, the muscles maintained maximal force, despite the fact that less SERCA2 in these fibres would be expected to lower the amount of Ca 2+ released during contraction, and thereby lower the maximal force. Our findings raise important questions regarding the roles of SERCA2 and SR in muscle function.