FIG. 7.

GSNOR-deficient skeletal muscles have normal mitochondrial content. Mitochondrial biogenesis was investigated as a potential mechanism that could contribute to enhanced GSNOR^−/− tibialis anterior (TA) muscle contractility. (A) Representative Western blot and densitometric quantitation of mitochondrial outer membrane VDAC1 protein expression in wild-type (+/+) and GSNOR^−/− TA muscles. (B) Representative Western blots and densitometric quantitation of expression of subunits of mitochondrial respiratory chain complexes I through V in wild-type and GSNOR^−/− TA muscles. Although complex II subunit SDHB expression was significantly higher in GSNOR^−/− TA muscle, expression of subunits from all other complexes was unaffected, arguing against biogenesis. *p < 0.05. (C) Citrate synthase activity, a biomarker of mitochondrial content, was similar between wild-type and GSNOR^−/− TA muscle. (D) The ratio of ND1/β-actin DNA was unaffected by GSNOR deficiency. (E) mRNA expression of PGC1α, an important transcriptional regulator of mitochondrial biogenesis, was similar between WT and GSNOR^−/− muscle. n = 6 for all groups.