title: COPD results in a reduction in UCP3 long mRNA and UCP3 protein content in types I and IIa skeletal muscle fibers.
abstract: OBJECTIVE
  Findings recently have shown coupling protein-3 (UCP3) content to be decreased in the skeletal muscle of patients with chronic obstructive pulmonary disease (COPD). Uncoupling protein-3 mRNA exists as two isoforms: long (UCP3L) and short (UCP3S). The UCP3 protein is expressed the least in oxidative and the most in glycolytic muscle fibers. Levels of UCP3 have been associated positively with intramyocellular triglyceride (IMTG) contents in conditions of altered fatty acid metabolism. As a source for muscle free fatty acid metabolism, IMTG is decreased in COPD. The current study completely characterized all the parameters of UCP3 expression (ie, UCP3L and UCP3S mRNA expression in whole muscle samples) and UCP3 protein content as well as IMTG content in the different fiber types in patients with COPD and healthy control subjects.
  
  
  METHODS
  Using real-time polymerase chain reaction, UCP3 gene expression was quantified. Skeletal muscle fiber type and UCP3 protein and IMTG content were measured using immunofluorescence and Oil red oil staining, respectively.
  
  
  RESULTS
  The findings showed that UCP3L mRNA expression was 44% lower (P < .005) in the patients with COPD than in the control subjects, whereas the UCP3S mRNA content was similar in the two groups. As compared with control subjects, UCP3 protein content was decreased by 89% and 83% and the IMTG content by 64% and 54%, respectively, in types I and IIa fibers (P < .0167) of patients with COPD, whereas they were unchanged in IIx fibers.
  
  
  CONCLUSIONS
  The reduced UCP3 and IMTG content in the more oxidative fibers may be linked to the altered muscle fatty acid metabolism associated with COPD. Further studies are required to determine the exact role and clinical relevance of the reduced UCP3 content in patients with COPD.
authors.affiliation: Clinique Romande de Réadaptation SUVA Care, Sion, Switzerland. aaron.russell@crr-suva.ch
authors.forename: Aaron P
authors.initials: AP
authors.lastname: Russell
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Somm
authors.forename: Richard
authors.initials: R
authors.lastname: Debigaré
authors.forename: Oliver
authors.initials: O
authors.lastname: Hartley
authors.forename: Denis
authors.initials: D
authors.lastname: Richard
authors.forename: Giacomo
authors.initials: G
authors.lastname: Gastaldi
authors.forename: Astrid
authors.initials: A
authors.lastname: Melotti
authors.forename: Annie
authors.initials: A
authors.lastname: Michaud
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Giacobino
authors.forename: Patrick
authors.initials: P
authors.lastname: Muzzin
authors.forename: Pierre
authors.initials: P
authors.lastname: LeBlanc
authors.forename: François
authors.initials: F
authors.lastname: Maltais
mesh_terms: D000368:Aged; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D016022:Case-Control Studies; D006801:Humans; D007473:Ion Channels; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000235:genetics / Q000378:metabolism; D024101:Mitochondrial Proteins; D018656:Muscle Fibers, Fast-Twitch / Q000378:metabolism*; D018657:Muscle Fibers, Slow-Twitch / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D000071247:Uncoupling Protein 3
chemical_list: D002352:Carrier Proteins; D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; C000604392:UCP3 protein, human; D000071247:Uncoupling Protein 3