scholarly journals Inhibitory effect of prostaglandin E2, forskolin, and dibutyryl cAMP on arachidonic acid release and inositol phospholipid metabolism in guinea pig neutrophils.

1986 ◽  
Vol 261 (3) ◽  
pp. 1092-1098 ◽  
Author(s):  
T Takenawa ◽  
J Ishitoya ◽  
Y Nagai
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Prostaglandin E2 ◽  
Inhibitory Effect ◽  
Phospholipid Metabolism ◽  
Arachidonic Acid Release ◽  
Dibutyryl Camp ◽  
Acid Release ◽  
Inositol Phospholipid

scholarly journals Relationship between arachidonic acid release and Ca2+-dependent exocytosis in digitonin-permeabilized bovine adrenal chromaffin cells

1990 ◽  
Vol 271 (3) ◽  
pp. 571-574 ◽  
Author(s):  
A Morgan ◽  
R D Burgoyne
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Chromaffin Cells ◽  
Nordihydroguaiaretic Acid ◽  
Inhibitory Effect ◽  
Arachidonic Acid Release ◽  
Adrenal Chromaffin Cells ◽  
Protein Kinase C Inhibitor ◽  
Acid Release ◽  
Adrenal Chromaffin

The relationship between Ca2(+)-dependent arachidonic acid release and exocytosis from digitonin-permeabilized bovine adrenal chromaffin cells was investigated. The phospholipase A2 inhibitors mepacrine, nordihydroguaiaretic acid and indomethacin had no effect on either arachidonic acid release or secretion. The phospholipase A2 activator melittin had no effect on secretion. The specific diacylglycerol lipase inhibitor RG80267 had no effect on secretion, but decreased basal arachidonic acid release to such an extent that the level of arachidonic acid in treated cells in response to 10 microM-Ca2+ was equivalent to that of control cells in the absence of Ca2+. Staurosporine, a protein kinase C inhibitor, was found to abolish Ca2(+)-dependent arachidonic acid release completely, but had only a slight inhibitory effect on Ca2(+)-dependent secretion. It is concluded that arachidonic acid is not essential for Ca2(+)-dependent exocytosis in adrenal chromaffin cells.

Studies on the action of dexamethasone on prostaglandin production by freshly dispersed amnion cells

1993 ◽  
Vol 128 (6) ◽  
pp. 563-567 ◽  
Author(s):  
William Gibb ◽  
Robert Breton
Keyword(s):  
Arachidonic Acid ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Inhibitory Effect ◽  
Arachidonic Acid Release ◽  
Dexamethasone Treatment ◽  
Glucocorticoid Treatment ◽  
Prostaglandin Production ◽  
Acid Release ◽  
Dispersed Cells

The human amnion may be an important source of prostaglandins (PGs) during pregnancy and possibly labor. Glucocorticoids stimulate PG production in confluent amnion cell cultures, but in freshly dispersed cells they inhibit PG production. The purpose of the present study was to determine if this inhibitory effect occurred at the level of arachidonic acid release from lipids. Cells were labeled with radioactive arachidonate and the release of radioactivity was measured in the presence or absence of dexamethasone. No significant effect of dexamethasone treatment was observed. The possibility that glucocorticoid treatment inhibited the release of arachidonate from a specific species of phospholipid was also examined. However, no difference was found in the distribution of arachidonate between lipids isolated from glucocorticoid-treated and untreated cells. Furthermore, dexamethasone treatment did not alter the lipocortin 1 and 2 content of dispersed cells, determined following sodium dodecyl sulfate polyacrylamide gel electrophoresis and immunoblotting. These studies indicate that the inhibition of prostaglandin production by dispersed amnion cells by glucocorticoids most likely occurs at a point distal to arachidonic acid release.

Sign in / Sign up

Export Citation Format

Share Document