TY - JOUR
TI - High glucose protects embryonic cardiac cells against simulated ischemia
AU - Malliopoulou, V.
AU - Xinaris, C.
AU - Mourouzis, I.
AU - Cokkinos, A.D.
AU - Katsilambros, N.
AU - Pantos, C.
AU - Kardami, E.
AU - Cokkinos, D.V.
JO - Molecular and Cellular Biochemistry
PY - 2006
VL - 284
TODO - 1-2
SP - 87-93
PB - 
SN - 0300-8177
TODO - 10.1007/s11010-005-9018-1
TODO - glucose;  iodoacetic acid;  propidium iodide;  protein kinase C delta;  protein kinase C epsilon;  glucose;  mitogen activated protein kinase 1;  mitogen activated protein kinase 3;  mitogen activated protein kinase p38;  protein kinase C delta;  protein kinase C epsilon, animal cell;  article;  cell culture;  cell death;  cell level;  chemoluminescence;  cytosol;  embryo;  embryo cell;  enzyme analysis;  glucose intake;  glucose metabolism;  glucose transport;  glycolysis;  heart muscle cell;  heart muscle ischemia;  heart protection;  hypoxia;  immunoreactivity;  nonhuman;  protein transport;  rat;  simulation;  Student t test;  Western blotting;  animal;  cell hypoxia;  cell line;  drug effect;  heart muscle cell;  heart muscle ischemia;  metabolism;  phosphorylation, Animals;  Cell Hypoxia;  Cell Line;  Glucose;  Mitogen-Activated Protein Kinase 1;  Mitogen-Activated Protein Kinase 3;  Myocardial Ischemia;  Myocytes, Cardiac;  p38 Mitogen-Activated Protein Kinases;  Phosphorylation;  Protein Kinase C-delta;  Protein Kinase C-epsilon;  Protein Transport;  Rats
TODO - In the present study we investigated whether acute glucose administration could be protective against hypoxic stress. H9c2 cells were exposed to either 4.5 mM or 22 mM of glucose for 15,min and then were submitted to simulated ischemia. Cell death was microscopically assessed by combined staining with propidium iodide (PI) and Hoeschst 33358. Intracellular content of glucose was measured by enzymatic analysis. Clucose content of H9c2 cells was 48.24 ± 7.94 μmol/L in the 22 mM vs 23.86 ± 4.8, μmol/L in the 4.5 mM group (p < 0.05). PKCε expression was increased 1.6 fold in the membrane fraction after pretreatment with high glucose (p < 0.05), while was decreased 1.6 fold in the cytosol (p < 0.05). In addition, no difference to PKCδ translocation was observed after pretreatment with low glucose. After hypoxia, in the 22 mM group, cell death was found to be 17.36 ± 2.66% vs 38.2± 5.4% in the 4.5 mM group (p < 0.05). In the presence of iodoacetic acid, a glycolytic inhibitor, cell death was not different between the two groups (23.54 ± 3.2% in 22 mM vs 22.06 ± 5.3% in 4.5 mM). Addition of chelerythrine did not change the protective effect of high glucose (13.4 ± 1.7% cell death in 22 mM vs 27.5 ± 5.5% in 4.5 mM, p < 0.05). In onclusion, short pretreatment with high glucose protects H9c2 cells against hypoxia. Although this protective effect is associated with translocation of PKCε and increased glucose uptake, it was abrogated only by inhibition of glycolysis. © Springer Science+Business Media, Inc. 2006.
ER -