It is now believed that PLD may contribute to the sustained generation of diacylglycerol (DAG) within activated cells. DAG can be formed from phosphatidylcholine by the sequential actions of PLD and phosphatidic acid phosphohydrolase. Phorbal myristate acetate (PMA, 1 microM), A23187 (10 microM) or platelet-activating factor (PAF, 100 nM) caused significant enhancement of intracellular 14C-phosphatidic acid levels 2-5 min after the addition of stimulus, in cultures of peritoneal macrophages pre-labelled with 14C-palmitate. Bacterial lipopolysaccharide (LPS) (5 micrograms/ml) or zymosan (375 micrograms/ml) also stimulated the production of 14C-phosphatidic acid, but over a longer time course (15-60 min). In the presence of 1% ethanol each stimulus caused significant production of 4C-phosphatidylethanol at the expense of 14C-phosphatidic acid, thus confirming a contribution of PLD in these reactions. This is the first report of PLD activity in this cell type.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/BF01972706 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Effect of ethanol on ATP-induced phospholipases C and D and serine base exchange in glioma C6 cells.
Neurochem Int
February 2000
Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
The effect of extracellular ATP, a nucleotide receptor agonist in the central nervous system, was investigated in glioma C6 cells on the intracellular Ca2+ level and the formation of phosphatidylethanol and phosphatidic acid in the presence and absence of ethanol (150 mM). In the cells prelabeled with [14C]palmitic acid, 100 microM ATP induced both the hydrolysis and the transphosphatidylation reactions leading to the formation of [14C]phosphatidic acid; addition of ethanol generated [14C]phosphatidylethanol. However, ATP-mediated increase in the level of [14C]phosphatidic acid was not inhibited by ethanol.
View Article and Find Full Text PDFPhospholipase A2-mediated activation of phospholipase D in rat heart sarcolemma.
J Mol Cell Cardiol
June 1998
Laboratory of Membrane Biology, St Boniface General Hospital Research Centre, Winnipeg, Canada.
The effect of phospholipase A2 (PLA2)-dependent release of unsaturated fatty acids (FA) on phospholipase D (PLD) function was examined in purified sarcolemmal (SL) membranes isolated from rat heart. PLD hydrolytic activity was determined by measuring either [14C] phosphatidic acid formation from exogenous [14C] phosphatidylcholine (PtdCho) or [3H] choline release from prelabelled SL Ptd[3H]choline. SL membranes with endogenous [3H] PtdCho that were prelabelled with [3H] myristic acid were used for testing PLD transphosphatidylation activity.
View Article and Find Full Text PDFFatty acid binding protein: stimulation of microsomal phosphatidic acid formation.
Arch Biochem Biophys
May 1997
Department of Physiology and Pharmacology, Texas A & M University 77843-4466, USA.
The effect of fatty acid binding proteins (FABPs) on two key steps of microsomal phosphatidic acid formation was examined. Rat liver microsomes were purified by size-exclusion chromatography to remove endogenous cytosolic fatty acid and fatty acyl-CoA binding proteins while recombinant FABPs were used to avoid cross-contamination with such proteins from native tissue. Neither rat liver (L-FABP) nor rat intestinal fatty acid binding protein (I-FABP) stimulated liver microsomal fatty acyl-CoA synthase.
View Article and Find Full Text PDFNitric oxide--a retrograde messenger for carbon monoxide signaling in ischemic heart.
Mol Cell Biochem
October 1996
Department of Surgery, University of Connecticut School of Medicine, Farmington 06030, USA.
To examine the intracellular signaling mechanism of NO in ischemic myocardium, isolated working rat hearts were made ischemic for 30 min followed by 30 min of reperfusion. A separate group of hearts were pre-perfused with 3 mM L-arginine in the presence or absence of 650 microM of protoporphyrin, a heme oxygenase inhibitor for 10 min prior to ischemia. The release of NO was monitored using an on-line amperometric sensor placed into the right atrium.
View Article and Find Full Text PDFNitric oxide signaling in ischemic heart.
Cardiovasc Res
October 1995
Department of Surgery, University of Connecticut School of Medicine, Farmington 06030-1110, USA.
Objective: Several recent studies have implicated a role of endogenous nitric oxide (NO) in the pathophysiology of myocardial ischemic/reperfusion injury. However, the mechanism by which NO exerts its beneficial/detrimental effects remains unknown. This study examined the intracellular signaling of NO by studying the role of the NO-cGMP signaling pathway on the phospho-diesteratic breakdown and turnover of phosphoinositides during myocardial ischemia and reperfusion.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!