دورية أكاديمية
أعرض في EDS

Altered expression of the adenine nucleotide translocase isoforms and decreased ATP synthase activity in skeletal muscle mitochondria in heart failure.

التفاصيل البيبلوغرافية
العنوان: Altered expression of the adenine nucleotide translocase isoforms and decreased ATP synthase activity in skeletal muscle mitochondria in heart failure.
المؤلفون: Rosca MG; Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4981, USA., Okere IA, Sharma N, Stanley WC, Recchia FA, Hoppel CL
المصدر: Journal of molecular and cellular cardiology [J Mol Cell Cardiol] 2009 Jun; Vol. 46 (6), pp. 927-35. Date of Electronic Publication: 2009 Feb 20.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: England NLM ID: 0262322 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-8584 (Electronic) Linking ISSN: 00222828 NLM ISO Abbreviation: J Mol Cell Cardiol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London, New York, Academic Press.
مواضيع طبية MeSH: Heart Failure/*metabolism , Mitochondrial ADP, ATP Translocases/*metabolism , Mitochondrial Proton-Translocating ATPases/*metabolism , Muscle, Skeletal/*enzymology , Protein Isoforms/*metabolism, Animals ; Citrate (si)-Synthase/metabolism ; Dogs ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Electron Transport Complex III/metabolism ; Electron Transport Complex IV/metabolism ; Heart Failure/pathology ; Immunoblotting ; Male ; Mitochondrial Membranes/metabolism ; Oxidative Phosphorylation
مستخلص: Exercise intolerance is a component of heart failure (HF) syndrome. We aimed to identify the defects in skeletal muscle mitochondria which may contribute to the development of peripheral myopathy. Subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria were isolated from gastrocnemius muscle of control dogs (N=5) and dogs with pacing-induced HF (N=5). The measurement of integrated mitochondrial function (oxidative phosphorylation) and of individual activities of mitochondrial electron transport chain (ETC) complexes was complemented with the assessment of the amount and activity of the components of the phosphorylation apparatus. Both populations of skeletal muscle mitochondria isolated from HF have significantly decreased ADP-stimulated (state 3) respiratory rates with complex I, II and III substrates. The decrease in respiratory rates of skeletal muscle SSM are neither relieved upon collapsing the mitochondrial potential with an uncoupler nor increased in the presence of maximal ADP concentrations showing a defect in the ETC, which needs further investigation. In contrast, respiratory rates of skeletal muscle IFM from HF were relieved with the uncoupler and partially improved in the presence of maximal ADP concentrations. In these IFM, alterations in the phosphorylation apparatus were detected with a decreased amount of ANT isoform 2 and increased amount of isoform 1. The IFM dysfunction may be explained by this shift in ANT isoforms. In conclusion, pacing-induced HF causes a decrease in the oxidative phosphorylation of skeletal muscle mitochondria due to defects in the ETC and phosphorylation apparatus.
معلومات مُعتمدة: P01 HL074237 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Protein Isoforms)
9068-80-8 (Mitochondrial ADP, ATP Translocases)
EC 1.3.5.1 (Electron Transport Complex II)
EC 1.9.3.1 (Electron Transport Complex IV)
EC 2.3.3.1 (Citrate (si)-Synthase)
EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases)
EC 7.1.1.2 (Electron Transport Complex I)
EC 7.1.1.8 (Electron Transport Complex III)
تواريخ الأحداث: Date Created: 20090224 Date Completed: 20090820 Latest Revision: 20191210
رمز التحديث: 20231215
DOI: 10.1016/j.yjmcc.2009.02.009
PMID: 19233197
قاعدة البيانات: MEDLINE
الوصف
تدمد:1095-8584
DOI:10.1016/j.yjmcc.2009.02.009