Anoxic injury accelerates phosphatidylcholine degradation in cultured cardiac myocytes by phospholipase C.
In neonatal cultured cardiac myocytes under normoxic conditions, 32Pi incorporation pattern into various phospholipids, and double-labeling experiments with 32Pi and [3H]methyl choline, suggest that phosphatidylcholine and phosphatidylinositol are turned over rapidly, whereas the turnover of phosphatidylethanolamine is probably much slower. While increased levels of the corresponding lysophospholipids were not found under anoxia, release of diacylglycerol and phosphorylcholine was observed. These data strongly suggest that phospholipase C, and not phospholipase A2, is involved in phospholipid degradation in cultured cardiomyocytes under anoxic conditions.
Nachas
N
N
Laboratory for Myocardial Research, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Pinson
A
A
D000818:Animals; D000831:Animals, Newborn; D001095:Arachidonic Acids / Q000378:metabolism; D002478:Cells, Cultured; D002794:Choline / Q000378:metabolism; D007700:Kinetics; D050356:Lipid Metabolism; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010100:Oxygen / Q000378:metabolism*; D010713:Phosphatidylcholines / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D010738:Type C Phospholipases / Q000378:metabolism*
D001095:Arachidonic Acids; D010713:Phosphatidylcholines; D010738:Type C Phospholipases; D002794:Choline; D010100:Oxygen