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Fig. 1 | Skeletal Muscle

Fig. 1

From: Failed upregulation of TFAM protein and mitochondrial DNA in oxidatively deficient fibers of chronic obstructive pulmonary disease locomotor muscle

Fig. 1

Higher prevalence of damaged protein and DNA in COPD vastus lateralis skeletal muscle. a Higher levels of 4-hydroxynonenal (HNE)-adduct containing proteins in COPD patients (0.85 ± 0.13; n = 17) compared to age-matched controls (0.43 ± 0.11; n = 10; *P < 0.05). b Higher concentration of oxidatively damaged guanosine (pg of 8-OHdG per uL of total DNA) in COPD muscle (386 ± 40.64; n = 29) compared to age-matched controls (258.0 ± 21.44; n = 16; *P < 0.01). c Representative image of long-range PCR gel demonstrating mtDNA deletions in COPD and control subjects. Lane 1: wild-type mtDNA taken from a young adult demonstrating the full-length (10.774 kb) amplified PCR product. Lane 2: mtDNA taken from a subject known to harbor a single mtDNA deletion resulting in an amplified product of 7.1 kb, thus demonstrating the specificity of this technique in detecting mtDNA deletions. Lanes 3–8, 16–25, and 28–29 show the presence of deletion-containing amplicons together with wild-type mtDNA product in most COPD subjects. Lanes 9–14 and 26–27 show the presence of the full-length wild-type mtDNA product and deletion-containing amplicons in control subjects. Graphs show mean ± SEM

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