scholarly journals Arachidonic acid release in rabbit neutrophils

1989 ◽  
Vol 257 (3) ◽  
pp. 633-637 ◽  
Author(s):  
W Tao ◽  
T F P Molski ◽  
R I Sha'afi
Keyword(s):  
Arachidonic Acid ◽  
Pertussis Toxin ◽  
Kinase Inhibitor ◽  
Regulatory Protein ◽  
Platelet Activating Factor ◽  
Arachidonic Acid Release ◽  
Membrane Perturbation ◽  
Acid Release ◽  
Guanine Nucleotide Regulatory Protein ◽  
Dose Dependent

[3H]Arachidonic acid is released after stimulation of rabbit neutrophils with fMet-Leu-Phe or platelet-activating factor (PAF). The release is rapid and dose-dependent, and is inhibited in phorbol 12-myristate 13-acetate (PMA)-treated rabbit neutrophils. The protein kinase C (PKC) inhibitor 1-(5-isoquinoline-sulphonyl)-2-methylpiperazine (H-7) prevents this inhibition. In addition, PMA increases arachidonic acid release in H-7-treated cells stimulated with fMet-Leu-Phe. [3H]Arachidonic acid release, but not the rise in the concentration of intracellular Ca2+, is inhibited in pertussis-toxin-treated neutrophils stimulated with PAF. The diacylglycerol kinase inhibitor R59022 increases the concentration of diacylglycerol and potentiates [3H]arachidonic acid release in neutrophils stimulated with fMet-Leu-Phe. This potentiation is not inhibited by H-7. These results suggest several points. (1) A rise in the intracellular concentration of free Ca2+ is not sufficient for arachidonic acid release in rabbit neutrophils stimulated by physiological stimuli. (2) A functional pertussis-toxin-sensitive guanine nucleotide regulatory protein and/or one or more of the changes produced by phospholipase C activation are necessary for arachidonic acid release produced by physiological stimuli. (3) Agents that stimulate PKC potentiate arachidonic acid release, and this potentiation is not inhibited by H-7. These agents produce their actions in part by direct membrane perturbation.

Tannin stimulates arachidonic acid release from bovine tracheal epithelial cells

1996 ◽  
Vol 270 (4) ◽  
pp. L613-L618
Author(s):  
M. M. Cloutier ◽  
L. Guernsey
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Pertussis Toxin ◽  
Condensed Tannin ◽  
Tracheal Epithelial Cells ◽  
Low Concentrations ◽  
Tracheal Epithelial ◽  
Acid Release ◽  
High Concentrations ◽  
Dose Dependent

Condensed tannin, isolated from cotton bracts extract (CBE), increases arachidonic acid (AA) release from rabbit alveolar macrophages and inhibits its subsequent reacylation. We determined whether tannin from CBE had any effect upon AA release in bovine tracheal epithelial cells (BTE). [14C] AA release was measured at timed intervals after addition of various concentrations of tannin to BTE cells grown to confluence in the presence of [14C] AA. Tannin caused a time- and dose-dependent release of AA from airway cells, with a maximum release occurring at 1 min in the presence of 100 micrograms/ml of tannin, and was confirmed by high-pressure liquid chromatography. The pattern of release was similar to that observed with bradykinin (2 x 10(-6) M). AA release by tannin was partially inhibited by indomethacin (10(-5) M) but not by 5,8,11,14-eicosatetraynoic acid (ETYA; 10(-5) M. Both of these drugs were effective in inhibiting bradykinin-induced AA release. In addition, AA release was not inhibited by cycloheximide. Endotoxin at 100 pg/ml and higher also caused a time-dependent release of AA that was not inhibitable by indomethacin or ETYA. Tannin-induced AA release was inhibited by pretreatment with pertussis toxin but not by neomycin, an inhibitor of phospholipase C (PLC). Neither pertussis toxin nor neomycin had any effect upon endotoxin-induced AA release. In other experiments, neither tannin nor endotoxin had any effect on [14C]AA uptake by BTE. These data demonstrate that tannin at low concentrations and endotoxin at high concentrations increase AA release by BTE cells. The AA release by tannin is partially metabolized by the cyclooxygenase pathway. We hypothesize that tannin-induced AA release is not mediated by PLC but may be mediated by other phospholipases, including PLA2.

scholarly journals Thrombin, unlike vasopressin, appears to stimulate two distinct guanine nucleotide regulatory proteins in human platelets

1986 ◽  
Vol 238 (1) ◽  
pp. 109-113 ◽  
Author(s):  
M D Houslay ◽  
D Bojanic ◽  
D Gawler ◽  
S O'Hagan ◽  
A Wilson
Keyword(s):  
Pertussis Toxin ◽  
Plasma Membranes ◽  
Regulatory Protein ◽  
Platelet Activating Factor ◽  
Phospholipid Metabolism ◽  
Human Platelets ◽  
Regulatory Proteins ◽  
Guanine Nucleotide ◽  
Gtpase Activity ◽  
Guanine Nucleotide Regulatory Protein

The thrombin-stimulated GTPase activity of human platelets was additive with respect to the GTPase stimulation effected by prostaglandin E1, but not with that stimulated by adrenaline, vasopressin and platelet-activating factor (PAF). Treatment of platelet membranes with pertussis toxin partially inhibited the thrombin-stimulated GTPase, but had no effect on the vasopressin-stimulated GTPase activity, whereas cholera toxin treatment had no effect on either of these stimulated GTPase activities. Thrombin, adrenaline and PAF, but not vasopressin, inhibited the adenylate cyclase activity of isolated plasma membranes through the action of Ni only, this being inhibited by pertussis toxin. It is suggested that thrombin exerts effects through both the inhibitory guanine nucleotide regulatory protein Ni and through the putative guanine nucleotide regulatory protein, Np, involved in regulating receptor-stimulated inositol phospholipid metabolism. However, vasopressin appears to exert its effects solely through the putative Np.

scholarly journals Mastoparan, a novel mitogen for Swiss 3T3 cells, stimulates pertussis toxin-sensitive arachidonic acid release without inositol phosphate accumulation.

1991 ◽  
Vol 113 (4) ◽  
pp. 943-950 ◽  
Author(s):  
J Gil ◽  
T Higgins ◽  
E Rozengurt
Keyword(s):  
Arachidonic Acid ◽  
Growth Factor ◽  
Dna Synthesis ◽  
Pertussis Toxin ◽  
Inositol Phosphate ◽  
Dependent Manner ◽  
Arachidonic Acid Release ◽  
3T3 Cells ◽  
Acid Release ◽  
Swiss 3T3

Mastoparan, a basic tetradecapeptide isolated from wasp venom, is a novel mitogen for Swiss 3T3 cells. This peptide induced DNA synthesis in synergy with insulin in a concentration-dependent manner; half-maximum and maximum responses were achieved at 14 and 17 microM, respectively. Mastoparan also stimulated DNA synthesis in the presence of other growth promoting factors including bombesin, insulin-like growth factor-1, and platelet-derived growth factor. The synergistic mitogenic stimulation by mastoparan can be dissociated from activation of phospholipase C. Mastoparan did not stimulate phosphoinositide breakdown, Ca2+ mobilization or protein kinase C-mediated phosphorylation of a major cellular substrate or transmodulation of the epidermal growth factor receptor. In contrast, mastoparan stimulated arachidonic acid release, prostaglandin E2 production, and enhanced cAMP accumulation in the presence of forskolin. These responses were inhibited by prior treatment with pertussis toxin. Hence, mastoparan stimulates arachidonic acid release via a pertussis toxin-sensitive G protein in Swiss 3T3 cells. Arachidonic acid, like mastoparan, stimulated DNA synthesis in the presence of insulin. The ability of mastoparan to stimulate mitogenesis was reduced by pertussis toxin treatment. These results demonstrate, for the first time, that mastoparan stimulates reinitiation of DNA synthesis in Swiss 3T3 cells and indicate that this peptide may be a useful probe to elucidate signal transduction mechanisms in mitogenesis.

scholarly journals Rifampin Inhibits Prostaglandin E2 Production and Arachidonic Acid Release in Human Alveolar Epithelial Cells

2007 ◽  
Vol 51 (12) ◽  
pp. 4225-4230 ◽  
Author(s):  
Yael Yuhas ◽  
Inbar Azoulay-Alfaguter ◽  
Eva Berent ◽  
Shai Ashkenazi
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Arachidonic Acid Release ◽  
Alveolar Epithelial ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Acid Release ◽  
Dose Dependent ◽  
Human Alveolar Epithelial Cells

ABSTRACT Rifampin, a potent antimicrobial agent, is a major drug in the treatment of tuberculosis. There is evidence that rifampin also serves as an immunomodulator. Based on findings that arachidonic acid and its metabolites are involved in the pathogeneses of Mycobacterium tuberculosis infections, we investigated whether rifampin affects prostaglandin E2 (PGE2) production in human alveolar epithelial cells stimulated with interleukin-1β. Rifampin caused a dose-dependent inhibition of PGE2 production. At doses of 100, 50, and 25 μg/ml, it inhibited PGE2 production by 75%, 59%, and 45%, respectively (P < 0.001). Regarding the mechanism involved, rifampin caused a time- and dose-dependent inhibition of arachidonic acid release from the alveolar cells. At doses of 100, 50, 25, and 10 μg/ml, it significantly inhibited the release of arachidonic acid by 93%, 64%, 58%, and 35%, respectively (P < 0.001). Rifampin did not affect the phosphorylation of cytosolic phospholipase A2 or the expression of cyclooxygenase-2. The inhibition of PGE2, and presumably other arachidonic acid products, probably contributes to the efficacy of rifampin in the treatment of tuberculosis and may explain some of its adverse effects.

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