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Skeletal muscle force is preserved in NOX4 deficient mice
Author(s) -
Frye Gregory,
Ahn Bumsoo,
Brandes Ralf P.,
Schröder Katrin,
Ferreira Leonardo F.
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.1075.12
Subject(s) - nox4 , nadph oxidase , skeletal muscle , medicine , endocrinology , chemistry , soleus muscle , gene isoform , knockout mouse , biochemistry , biology , reactive oxygen species , receptor , gene
NADPH oxidase levels are elevated in various cardiovascular diseases. The NOX4 isoform of NADPH oxidase generates reactive oxygen species that promotes calcium release in skeletal muscle. NOX4 knockdown depresses maximal tetanic force in mouse EDL muscle. We tested the hypotheses that NOX4 deficient mice would have decreased muscle force, rightward shift in the force‐frequency relationship, and accelerated fatigue in vitro. We studied intact soleus muscle from genetic control (C57BL/6J) and NOX 4 knockout mice (n = 7/group; 2 males/group) at 95%O2 and 37°C. Our initial experiments suggest no difference in maximal soleus tetanic force (Po) between groups (in N/cm2; Control 32 ± 6, NOX 4−/− 36 ± 4). Neither the stimulus frequency that elicited 50% Po (Control 53 ± 3 Hz; NOX4−/− 53 ± 8 Hz) nor muscle fatigue (not shown) was affected by NOX4 deficiency. Our study suggests that skeletal muscle force is preserved in mice lacking NOX4 isoform of NADPH oxidase.