Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rates of synthesis and degradation of heart protein were measured during 30 or 60 min of myocardial ischemia and during the 30 or 60 min following these ischemic periods. During ischemia, rates of protein synthesis and degradation were reduced. Resumption of control rates of coronary flow after 30 min of ischemia resulted in complete restoration of creatine phosphate and partial recovery of ATP (75%), developed pressure (79%), and cardiac output (80%). After 60 min of ischemia, restoration of flow completely restored creatine phosphate but resulted in poor recovery of ATP (57%), developed pressure (26%), and cardiac output (63%). During the recovery phase, rates of protein synthesis and degradation of protein to free amino acids were the same as in hearts that had been perfused for a comparable period as working aerobic preparations. These findings were consistent with inhibition of an initial step in proteolysis during the period of ischemia followed by return to control rates of degradation when oxygen delivery and energy levels were restored.
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PMID:Protein degradation and synthesis during recovery from myocardial ischemia. 721 59

PKC-delta is believed to play an essential role in cardiomyocyte growth. In the present study, we investigated the effect of PKC-delta on cardiac metabolism using PKC-delta knockout mice generated in our laboratories. Proteomic analysis of heart protein extracts revealed profound changes in enzymes related to energy metabolism: certain isoforms of glycolytic enzymes, e.g., lactate dehydrogenase and pyruvate kinase, were absent or decreased, whereas several enzymes involved in lipid metabolism, e.g., phosphorylated isoforms of acyl-CoA dehydrogenases, showed a marked increase in PKC-delta(-/-) hearts. Moreover, PKC-delta deficiency was associated with changes in antioxidants, namely, 1-Cys peroxiredoxin and selenium-binding protein 1, and posttranslational modifications of chaperones involved in cytoskeleton regulation, such as heat shock protein (HSP)20, HSP27, and the zeta-subunit of the cytosolic chaperone containing the T-complex polypeptide 1. High-resolution NMR analysis of cardiac metabolites confirmed a significant decrease in the ratio of glycolytic end products (alanine + lactate) to end products of lipid metabolism (acetate) in PKC-delta(-/-) hearts. Taken together, our data demonstrate that loss of PKC-delta causes a shift from glucose to lipid metabolism in murine hearts, and we provide a detailed description of the enzymatic changes on a proteomic level. The consequences of these metabolic alterations on sensitivity to myocardial ischemia are further explored in the accompanyingpaper (20).
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PMID:Loss of PKC-delta alters cardiac metabolism. 1527 8