Effect of calcium ionophore A23187 on electrogenic acid-base transport in turtle bladder Inhibition of acidification and stimulation of alkalinization

1983 ◽  
Vol 732 (1) ◽  
pp. 146-153 ◽  
Author(s):  
Gerhard Ehrenspeck
Keyword(s):  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Acid Base ◽  
Turtle Bladder ◽  
Bladder Inhibition ◽  
Stimulation Of

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.

Stimulation of AIDS lymphocytes with calcium ionophore (A23187) and phorbol ester (PMA): Studies of cytoplasmic free Ca, IL-2 receptor expression, IL-2 production and proliferation

1989 ◽  
Vol 119 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Bo Hofmann ◽  
Jarl Moller ◽  
Erik Langhoff ◽  
Klaus Damgård Jakobsen ◽  
Niels Odum ◽  
...  
Keyword(s):  
Phorbol Ester ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Receptor Expression ◽  
Ionophore A23187 ◽  
Stimulation Of

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.

Role of calcium in the secretomotor response of the thyroid: effects of calcium ionophore A23187 on radioiodine turnover, membrane potential and fluid transport in cultured porcine thyroid cells

1988 ◽  
Vol 116 (3) ◽  
pp. 373-380 ◽  
Author(s):  
S. W. Manley ◽  
D. S. Rose ◽  
G. J. Huxham ◽  
J. R. Bourke
Keyword(s):  
Calcium Concentration ◽  
Fluid Transport ◽  
Calcium Ionophore ◽  
Feedback Mechanism ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Thyroid Cells ◽  
Negative Feedback Mechanism ◽  
Stimulation Of

ABSTRACT The calcium ionophore A23187 (0·1–1 μmol/l) inhibited membrane electrical polarization, uptake of 125I, fluid transport and TSH-stimulated release of radioiodine from the organic pool in follicular cultures of porcine thyroid cells. At higher concentrations (1–30 μmol/l), A23187 promoted release of radioiodine from the organic pool. Stimulation of release of radioiodine from the organic pool by veratridine (a sodium channel agonist, 0·4–1 mmol/l) and A23187 was dependent on the calcium concentration of the medium, while TSH action was independent. Incubation in medium of very low calcium concentration (0·0177 mmol/l) resulted in enhanced release from the organic pool, which was inhibited by TSH (256 μU/ml), A23187 (25 μmol/l) or veratridine (0·5 mmol/l). These data therefore do not support the hypothesis that calcium acts as a mediator of the secretomotor action of TSH, but suggest the possibility of a TSH-induced increase in intracellular calcium as a regulatory negative-feedback mechanism. J. Endocr. (1988) 116, 373–380

Sign in / Sign up

Export Citation Format

Share Document