Scandinavian journal of rheumatology · 1999
Absence of mitochondrial dysfunction in polymyalgia rheumatica. Evidence based on a simultaneous molecular and biochemical approach.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Miró O, Jarreta D, Casademont J, Barrientos A, Rodríguez B, Gómez M, Nunes V, Urbano-Márquez A, Cardellach F
Аннотация
OBJECTIVE: To investigate the molecular and biochemical profile of skeletal muscle mitochondria of patients with isolated polymyalgia rheumatica (PMR).
PATIENTS AND METHODS: We included patients with a recent diagnosis of PMR and as control healthy individuals submitted to orthopedic surgery. Skeletal muscle was obtained from quadriceps, thus was mitochondria immediately isolated. Long polymerase chain reaction and Southern blot transference were performed to detect deleted mtDNA molecules. Mitochondrial oxidative activity using different substrates and individual enzyme activity of respiratory chain complexes were assessed to search for any biochemical dysfunction.
RESULTS: Fifty-one individuals (PMR=25, controls=26) were included. Mean age was 72 (11) years; 45% were females. We found no significant increase of deleted mtDNA molecules in PMR patients compared to controls. Both groups differed neither on oxygen consumption (p=NS for all substrates) nor enzymatic activity (p=NS for all complexes).
CONCLUSIONS: Skeletal muscle mitochondria are molecularly and biochemically unaffected in PMR.
PATIENTS AND METHODS: We included patients with a recent diagnosis of PMR and as control healthy individuals submitted to orthopedic surgery. Skeletal muscle was obtained from quadriceps, thus was mitochondria immediately isolated. Long polymerase chain reaction and Southern blot transference were performed to detect deleted mtDNA molecules. Mitochondrial oxidative activity using different substrates and individual enzyme activity of respiratory chain complexes were assessed to search for any biochemical dysfunction.
RESULTS: Fifty-one individuals (PMR=25, controls=26) were included. Mean age was 72 (11) years; 45% were females. We found no significant increase of deleted mtDNA molecules in PMR patients compared to controls. Both groups differed neither on oxygen consumption (p=NS for all substrates) nor enzymatic activity (p=NS for all complexes).
CONCLUSIONS: Skeletal muscle mitochondria are molecularly and biochemically unaffected in PMR.
Предметные рубрики MeSH
Adenosine TriphosphatasesAgedCarrier ProteinsDNA, MitochondrialElectron Transport Complex IIElectron Transport Complex IIIElectron Transport Complex IVFemaleHumansMaleMembrane ProteinsMitochondria, MuscleMitochondrial Proton-Translocating ATPasesMultienzyme ComplexesMuscle, SkeletalOxidative PhosphorylationOxidoreductasesOxygen ConsumptionPolymerase Chain ReactionPolymyalgia RheumaticaReference ValuesSequence DeletionSuccinate Dehydrogenase