Effect of ganglioside GM1 on arachidonic acid release in bovine aortic endothelial cells

Life Sciences ◽  
1994 ◽  
Vol 54 (1) ◽  
pp. 49-60 ◽  
Author(s):  
Joseph P. Bressler ◽  
Luisa Belloni-Olivi ◽  
Sheila Forman
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Arachidonic Acid Release ◽  
Ganglioside Gm1 ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Acid Release ◽  
Aortic Endothelial

Effects of Dipyrone on Prostaglandin Production by Human Platelets and Cultured Bovine Aortic Endothelial Cells

1983 ◽  
Vol 49 (02) ◽  
pp. 132-137 ◽  
Author(s):  
A Eldor ◽  
G Polliack ◽  
I Vlodavsky ◽  
M Levy
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Competitive Inhibition ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

SummaryDipyrone and its metabolites 4-methylaminoantipyrine, 4-aminoantipyrine, 4-acetylaminoantipyrine and 4-formylaminoan- tipyrine inhibited the formation of thromboxane A2 (TXA2) during in vitro platelet aggregation induced by ADP, epinephrine, collagen, ionophore A23187 and arachidonic acid. Inhibition occurred after a short incubation (30–40 sec) and depended on the concentration of the drug or its metabolites and the aggregating agents. The minimal inhibitory concentration of dipyrone needed to completely block aggregation varied between individual donors, and related directly to the inherent capacity of their platelets to synthesize TXA2.Incubation of dipyrone with cultured bovine aortic endothelial cells resulted in a time and dose dependent inhibition of the release of prostacyclin (PGI2) into the culture medium. However, inhibition was abolished when the drug was removed from the culture, or when the cells were stimulated to produce PGI2 with either arachidonic acid or ionophore A23187.These results indicate that dipyrone exerts its inhibitory effect on prostaglandins synthesis by platelets or endothelial cells through a competitive inhibition of the cyclooxygenase system.

Hypotonic stress-induced dual Ca2+ responses in bovine aortic endothelial cells

2000 ◽  
Vol 279 (2) ◽  
pp. H630-H638 ◽  
Author(s):  
Masahiro Oike ◽  
Chiwaka Kimura ◽  
Tetsuya Koyama ◽  
Miyuki Yoshikawa ◽  
Yushi Ito
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Receptor Antagonist ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Luciferase Assay ◽  
Aortic Endothelial Cells ◽  
Hypotonic Stress ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

We have investigated the effects of hypotonic stress on intracellular calcium concentration ([Ca2+]i) in bovine aortic endothelial cells. Reducing extracellular osmolarity by 5% to 40% elicited a steep Ca2+ transient both in normal Krebs and Ca2+-free solutions. The hypotonic stress-induced Ca2+ transient was inhibited by phospholipase C inhibitors (neomycin and U-73122), a P2-receptor antagonist (suramin), and an ATP-hydrolyzing enzyme (apyrase), suggesting that the hypotonic stress-induced Ca2+ transient is mediated by ATP. A luciferin-luciferase assay confirmed that 40% hypotonic stress released 91.0 amol/cell of ATP in 10 min. When the hypotonic stress-induced fast Ca2+ transient was inhibited by neomycin, suramin, or apyrase, a gradual [Ca2+]i increase was observed instead. This hypotonic stress-induced gradual [Ca2+]iincrease was inhibited by a phospholipase A2 inhibitor, 4-bromophenacyl bromide. Furthermore, exogenously applied arachidonic acid induced a gradual [Ca2+]i increase with an ED50 of 13.3 μM. These observations indicate that hypotonic stress induces a dual Ca2+ response in bovine aortic endothelial cells, i.e., an ATP-mediated fast Ca2+transient and an arachidonic acid-mediated gradual Ca2+increase, the former being the predominant response in normal conditions.

scholarly journals Arachidonic acid-induced Ca2+ transient in bovine aortic endothelial cells.

1999 ◽  
Vol 79 ◽  
pp. 171
Author(s):  
Miyuki Yoshikawa ◽  
Tetsuya Koyama ◽  
Chiwaka Kimura ◽  
Masahiro Oike ◽  
Yushi Ito
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

Effect of hypoxia on steady-state arachidonic acid metabolism in bovine aortic endothelial cells

1997 ◽  
Vol 272 (3) ◽  
pp. H1426-H1436 ◽  
Author(s):  
G. M. Patton ◽  
H. Kadowaki ◽  
H. Albadawi ◽  
H. M. Soler ◽  
M. T. Watkins
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Molecular Species ◽  
Specific Activity ◽  
Acute Hypoxia ◽  
Arachidonic Acid Metabolism ◽  
Eicosanoid Synthesis ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

At the onset of acute hypoxia, eicosanoid synthesis by bovine aortic endothelial cells (BAEC) markedly decreases, reflecting a decreased release of arachidonic acid from endogenous stores. To determine the cause of decreased arachidonic acid release, we pulse-labeled BAEC with [14C]arachidonic acid for 5 min under normoxic conditions and chased cells for 1 h under normoxic or hypoxic conditions. The 14C incorporation and specific activity (disintegrations per minute per nanomole) of three major arachidonyl molecular species (16:0-20:4, 18:1-20:4, and 18:0-20:4) of each phospholipid class were determined in cells chased under either of the two conditions. There was no relevant difference between normoxic and hypoxic cells in the metabolism of any of the arachidonyl molecular species of diacyl lipids. However, there was a marked decrease (approximately 40%) in the turnover of arachidonyl alkenylacyl phosphatidylethanolamine in the hypoxic cells. From these results, it appears that the source of arachidonic acid supporting constitutive eicosanoid synthesis in BAEC is alkenylacyl phosphatidylethanolamine and that the limiting enzyme activity determining the rate of eicosanoid synthesis is a plasmalogen-specific phospholipase A2.

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