Mitochondrial and sarcoplasmic protein changes in hearts from copper-deficient rats: up-regulation of PGC-1alpha transcript and protein as a cause for mitochondrial biogenesis in copper deficiency.

Changes in mitochondrial and sarcoplasmic proteins using proteinomics and Western blotting in hearts from copper-deficient rats were explored in this study. Also, key enzymes that are involved in cardiac energy metabolism via glycolysis and fatty acid oxidation and related transcription factors were...

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Published in:Journal of Nutritional Biochemistry Vol. 20; no. 10; pp. 823 - 831
Main Authors: Medeiros DM, Jiang Y, Klaahsen D, Lin D, Medeiros, Denis M, Jiang, Yu, Klaahsen, Darcey, Lin, Dingbo
Format: research Journal Article
Published: Elsevier B.V. Oct2009
Online Access:View this record in EBSCOhost
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      dt: Oct2009
      vid: 20
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      pub: Elsevier B.V.
      place: New York, New York
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        10.1016/j.jnutbio.2008.08.001
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        atl: Mitochondrial and sarcoplasmic protein changes in hearts from copper-deficient rats: up-regulation of PGC-1alpha transcript and protein as a cause for mitochondrial biogenesis in copper deficiency.
      aug:
        au:
          Medeiros DM
          Jiang Y
          Klaahsen D
          Lin D
          Medeiros, Denis M
          Jiang, Yu
          Klaahsen, Darcey
          Lin, Dingbo
        affil: Department of Human Nutrition, Kansas State University, Manhattan, KS 66506, USA
      sug:
        subj:
          Biochemical Phenomena
          Copper Deficiency
          Cytoplasm Metabolism
          Mitochondria Metabolism
          Muscle Proteins Metabolism
          Proteins Metabolism
          RNA
          Animal Studies
          Blotting, Western
          DNA Probes
          Electrophoresis
          Male
          Nucleotides
          Polymerase Chain Reaction
          Proteins
          Rats
          Male
      ab: Changes in mitochondrial and sarcoplasmic proteins using proteinomics and Western blotting in hearts from copper-deficient rats were explored in this study. Also, key enzymes that are involved in cardiac energy metabolism via glycolysis and fatty acid oxidation and related transcription factors were determined. Rats were fed one of two diets: a copper-adequate diet containing 6 mg Cu/kg diet or a diet with less than 1 mg Cu/kg diet for 5 weeks. Copper deficiency was confirmed by low liver copper levels, decreased hematocrit levels and cardiac hypertrophy. Proteinomic data revealed that of the more than 50 proteins identified from the mitochondrial fraction of heart tissue, six were significantly down-regulated and nine were up-regulated. The proteins that were decreased were beta enolase 3, carbonic anhydrase 2, aldose reductase 1, glutathione peroxidase, muscle creatine kinase and mitochondrial aconitase 2. The proteins that were up-regulated were isocitrate dehydrogenase, dihydrolipoamide dehydrogenase, transferrin, subunit d of ATP synthase, transthyretin, preproapolipoprotein A-1, GRP 75, alpha-B crystalline and heat shock protein alpha. Follow-up Western blots on rate-limiting enzymes in glycolysis (phosphofructose kinase), fatty acid oxidation (medium chain acyl dehydrogenase, peroxisome proliferator-actvator receptor-alpha or PPARalpha) and gluconeogenesis (phosphoenolpyruvate carboxykinase) did not reveal changes in metabolic enzymes. However, a significant increase in peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha protein, as well as the transcript, which increased 2.5-fold, was observed. It would appear that increased mitochondrial biogenesis known to occur in copper deficiency hearts is caused by an increased expression in the master regulator of mitochondrial biogenesis, PGC-1alpha.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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