Is there cross-refractoriness between phospholipase A2 and the calcium ionophore A23187 in the stimulation of uterine prostaglandin production?

1993 ◽  
Vol 48 (4) ◽  
pp. 327-330 ◽  
Author(s):  
N.L. Poyser ◽  
A. Ferguson
Keyword(s):  
Phospholipase A2 ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Prostaglandin Production ◽  
Stimulation Of

Tobacco smoke releases performed mediators from canine mast cells and modulates prostaglandin production

1992 ◽  
Vol 263 (1) ◽  
pp. L67-L72
Author(s):  
P. S. Thomas ◽  
R. E. Schreck ◽  
S. C. Lazarus
Keyword(s):  
Mast Cells ◽  
Tobacco Smoke ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Prostaglandin D2 ◽  
Ionophore A23187 ◽  
Temperature Dependent ◽  
Prostaglandin Production ◽  
Lungs And Airways

The role of an extract of tobacco smoke in activating mast cells was studied. With the use of isolated, canine mast cells as a model, we found that cigarette smoke solution (CSS) induced the release of the performed mediators histamine and tryptase from these cells in an energy- and temperature-dependent, non-cytotoxic manner. There was no requirement for extracellular calcium. Nicotine tartrate did not reproduce the effect of CSS. Interestingly, mast cells produced little prostaglandin D2 (PGD2) in response to the CSS, and there was a concentration-related inhibition of calcium ionophore A23187-induced PGD2 synthesis. This suggests at least two mechanisms acting on the mast cell: tobacco smoke can directly activate mast cells to release performed mediators and can simultaneously inhibit prostaglandin production. These observations suggest a mechanism by which mast cells may participate in the bronchospastic and proinflammatory changes seen in the lungs and airways of smokers.

Differential control of type-I iodothyronine deiodinase expression by the activation of the cyclic AMP and phosphoinositol signalling pathways in cultured human thyrocytes

1995 ◽  
Vol 14 (2) ◽  
pp. 171-177 ◽  
Author(s):  
S G Beech ◽  
S W Walker ◽  
J R Arthur ◽  
D Lee ◽  
G J Beckett
Keyword(s):  
Cyclic Amp ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Signalling Pathways ◽  
Cell Labelling ◽  
Ionophore A23187 ◽  
Type I ◽  
Iodothyronine Deiodinase ◽  
Differential Control ◽  
Stimulation Of

ABSTRACT The effects of TSH and the activation of the cyclic AMP (cAMP) and Ca2+-phosphatidylinositol (Ca2+-PI) cascades on the activity and expression of the selenoenzyme thyroidal type-I iodothyronine deiodinase (ID-I) have been studied using human thyrocytes grown in primary culture. Stimulation of ID-I activity and expression was obtained with TSH and an analogue of cAMP, 8-bromo-cAMP. In the presence or absence of TSH, the addition of the phorbol ester, phorbol 12-myristate 13-acetate (PMA) together with the calcium ionophore A23187, caused a decrease in ID-I activity; a decrease in ID-I expression was also observed as assessed by cell labelling with [75 Se]selenite. PMA alone had no effect on ID-I activity in the presence or absence of TSH. A23187 alone produced a small but significant reduction in ID-I activity, but only in TSH-stimulated cells. These data provide evidence that the expression of thyroidal ID-I is negatively regulated by the Ca2+-PI cascade, and positively regulated by the cAMP cascade.

Elevated extracellular K+ enhances arachidonic acid release in MDCK-D1 cells

1990 ◽  
Vol 259 (2) ◽  
pp. C224-C231 ◽  
Author(s):  
M. J. Howard ◽  
P. A. Insel
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Mdck Cells ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Membrane Receptors ◽  
Phosphoinositide Hydrolysis ◽  
Ionophore A23187 ◽  
K Concentration ◽  
The Impact

Depolarization can alter the expression of membrane receptors and change certain receptor-mediated events, but previous studies have not assessed the impact of depolarization on generation of arachidonic acid and its metabolites (AA) in nonexcitable tissues. We assessed AA generation in Madin-Darby canine kidney (MDCK) cells grown for 3 days in increased extracellular [K+], which is known to acutely depolarize these cells. Growth under these conditions resulted in decreases in the number of alpha 1-adrenergic receptors (alpha 1 AR), a small decrease in receptor-mediated phosphoinositide hydrolysis, but increases in alpha 1 AR-mediated prostaglandin E2 formation and AA release. Calcium ionophore (A23187)-, melittin-, and bradykinin-stimulated AA release were also enhanced. The reduction in alpha 1 AR number and increased AA release were substantially reduced or eliminated when K(+)-treated cells were grown in the absence of extracellular calcium. The results provide evidence that hormone-stimulated AA release and prostaglandin production can be enhanced by chronic exposure to elevated extracellular K+ concentration, perhaps as a consequence of a depolarization-induced enhancement in phospholipase A2 activity. The results provide evidence for the parallel and independent regulation of the pathways for receptor-mediated phosphoinositide hydrolysis (phospholipase C activation) and AA release (phospholipase A2 activation) in MDCK cells.

scholarly journals Stimulation of CEACAM1 expression by 12- O -tetradecanoylphorbol-13-acetate (TPA) and calcium ionophore A23187 in endometrial carcinoma cells

2005 ◽  
Vol 27 (3) ◽  
pp. 483-490 ◽  
Author(s):  
Ana-Maria Bamberger ◽  
Juliane Briese ◽  
Julica Götze ◽  
Insa Erdmann ◽  
Heinrich M. Schulte ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Carcinoma Cells ◽  
Ionophore A23187 ◽  
Stimulation Of

scholarly journals Early plasma-membrane-potential changes during stimulation of lymphocytes by concanavalin A.

1983 ◽  
Vol 210 (3) ◽  
pp. 885-891 ◽  
Author(s):  
S M Felber ◽  
M D Brand
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Concanavalin A ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
K Channel ◽  
Ionophore A23187 ◽  
Resting Cells ◽  
Plasma Membrane Potential ◽  
Stimulation Of

1. We have monitored the plasma-membrane potential of lymphocytes by measuring the accumulation of the lipophilic cation methyltriphenylphosphonium (TPMP+) in the presence of the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP). 2. The mitogen concanavalin A causes a decrease in TPMP+ accumulation by pig lymphocytes corresponding to a 3 mV depolarization with 2 1/2 min. Concanavalin A does not alter 86Rb+ uptake in the first 30 min. 3. In contrast concanavalin A increased TPMP+ accumulation and the rate of Rb+ uptake in mouse thymocytes. This is consistent with a previous proposal that the mitogen induces a hyperpolarization of mouse thymocytes as a result of stimulation of a Ca2+-dependent K+ channel. 4. Studies with the calcium ionophore A23187 and quinine (an inhibitor of the Ca2+-dependent K+ channel) suggest that the channel is partially closed in mouse resting thymocytes but is almost fully active in pig resting cells. Thus concanavalin A hyperpolarizes mouse thymocytes by activating the Ca2+-dependent K+ channel but cannot do so in pig lymphocytes because the channel is already maximally activated. 5. The 3mV depolarization of pig cells cannot be explained by a decrease in electrogenic K+ permeability.

Mechanisms of Nonimmunological Histamine and Tryptase Release from Human Cutaneous Mast Cells

2000 ◽  
Vol 92 (4) ◽  
pp. 1074-1081 ◽  
Author(s):  
Mette Veien ◽  
Fania Szlam ◽  
Jeannine T. Holden ◽  
Koji Yamaguchi ◽  
Donald D. Denson ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Phospholipase A2 ◽  
Histamine Release ◽  
Phospholipase C ◽  
Cell Activation ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Mast Cell Activation ◽  
Ionophore A23187

Background If mast cells are stimulated they release multiple mediators that delineate markers for immunologic and nonimmunologic reactions; histamine and tryptase are the two best known. Although histamine can be assayed in plasma, it is a nonspecific marker with a very short half-life. Tryptase has a longer half-life, but its release has not been proven to be specific for anaphylaxis. The authors investigated the mechanisms of nonimmunologic histamine release from human cutaneous mast cells to understand the mechanisms of mediator release and to determine whether tryptase was specific for allergic mediated activation. Methods Dispersed mast cell suspensions isolated from neonatal foreskins underwent challenge with vancomycin, calcium ionophore A23187, morphine, and atracurium, and histamine tryptase release was measured. The effects of calcium and magnesium, along with phospholipase C and phospholipase A2 inhibitors, also were investigated. Results Tryptase and histamine both were released by the known nonimmunologic stimuli (pharmacologic agents used in the current study; r2 = 0.6). Furthermore, vancomycin- and atracurium-induced histamine release was calcium dependent. Phospholipase C and phospholipase A2 inhibitors decreased vancomycin-induced histamine release, but not calcium ionophore A23187-induced release. Conclusions Tryptase is not a specific marker of mast cell activation (ie., anaphylaxis), and signaling mechanisms for mast cell activation involve activation of phospholipase C and phospholipase A2 pathways that are also involved in other cellular activation mechanisms.

Sign in / Sign up

Export Citation Format

Share Document