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Calcium ionophore A23187 induces expression of glucose-regulated genes and their heterologous fusion genes.

ABSTRACT: Using two cDNA clones which encode hamster genes specifically induced by glucose starvation, we demonstrated that an 8- and 30-fold increase, respectively, in the transcription rates of these genes was coordinately effected by calcium ionophore A23187 treatment, resulting in a similar increase in the steady-state levels of their mRNAs. This response was observed within several hours of ionophore treatment in several mammalian cell types and appeared to be specifically mediated by A23187 but not by other ionophores in general. To define the regulatory sequence which mediates this Ca2+-induced response, we showed by gene transfection techniques that the 5' flanking sequence of a rat glucose-regulated gene contained the region for induction by A23187. The system reported here offers attractive features for the study of specific gene regulation by Ca2+.

SUBMITTER: Resendez E

PROVIDER: S-EPMC366848 | biostudies-literature | 1985 Jun

REPOSITORIES: biostudies-literature

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Calcium ionophore A23187 induces expression of glucose-regulated genes and their heterologous fusion genes.

Resendez E E Attenello J W JW Grafsky A A Chang C S CS Lee A S AS

Molecular and cellular biology 19850601 6

Using two cDNA clones which encode hamster genes specifically induced by glucose starvation, we demonstrated that an 8- and 30-fold increase, respectively, in the transcription rates of these genes was coordinately effected by calcium ionophore A23187 treatment, resulting in a similar increase in the steady-state levels of their mRNAs. This response was observed within several hours of ionophore treatment in several mammalian cell types and appeared to be specifically mediated by A23187 but not ...[more]

PMID: 3929069

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Calcium ionophore A23187 induces release of chemokinetic and aggregating factors from polymorphonuclear leucocytes.

Project description:1. Rat and human polymorphonuclear leucocytes (PMNs) when exposed to calcium ionophore A23187 10 microM release products which cause aggregation of rat PMNs and chemokinesis of human PMNs. 2. Aggregating and chemokinetic activities are rapidly generated; maximal release occurs after 4 min, and can be detected in dilutions of the supernatant of up to 1:1000. 3. Generation of aggregating and chemokinetic activities is inhibited by nordihydroguaiaretic acid 10(-4) to 10(0-7) M, 5,8,11,14-eicosatetraynoic acid 10(-4) and 10(-5) M, BW 755C 10(-4) M and benoxaprofen 10(-4) M, all compounds known to inhibit lipoxygenase pathways of arachidonic acid (AA) metabolism. 4. Conventional non-steroidal anti-inflammatory agents, such as aspirin and indomethacin, inhibited little or not at all the generation of these activities. 5. We conclude that the aggregating and chemokinetic activities induced by A23187 represent generation of biologically active products of lipoxygenase pathways of AA metabolism.

| S-EPMC2044478 | biostudies-other

Calcium Ionophore (A23187) Rescues the Activation of Unfertilized Oocytes After Intracytoplasmic Sperm Injection and Chromosome Analysis of Blastocyst After Activation.

Project description:Calcium is a crucial factor in regulating the biological behavior of cells. The imbalance of calcium homeostasis in cytoplasm will cause abnormal behavior of cells and the occurrence of diseases. In intracytoplasmic sperm injection (ICSI) cycle, the dysfunction of oocyte activation caused by insufficient release of Ca2+ from endoplasmic reticulum is one of the main reasons for repeated fertilization failure. Calcium ionophore (A23187) is a highly selective calcium ionophore, which can form stable complex with Ca2+ and pass through the cell membrane at will, effectively increasing intracellular Ca2+ levels. It has been reported that calcium ionophore (A23187) can activate oocytes and obtain normal embryos. However, there are few studies on unfertilized oocytes after calcium ionophore (A23187) rescue activation in ICSI cycle. The purpose of this study was to analyze the effects of calcium ionophore (A23187) rescue activation on the activation of unfertilized oocytes, embryonic development potential, embryonic development timing and chromosomal aneuploidy, and to compare and analyze the clinical data of patients with calcium ionophore (A23187) activation in clinical application. The results showed that a certain proportion of high-quality blastocysts with normal karyotype could be obtained after calcium ionophore (A23187) rescue activation of unfertilized oocytes, and it did not have a significant effect on the timing of embryo development. In clinical practice, direct activation with calcium ionophore (A23187) after ICSI was better than rescue activation the next day. In conclusions, the studies on the effectiveness and safety of calcium ionophore (A23187) rescue activation for oocytes with ICSI fertilization failure can enable some patients to obtain usable, high-quality embryos during the first ICSI cycle.

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The calcium ionophore A23187 induces endothelium-dependent contractions in femoral arteries from rats with streptozotocin-induced diabetes.

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| S-EPMC2189770 | biostudies-other

The calcium ionophore A23187 increases the tight-junctional permeability in rat liver.

Project description:The effect of an increase in intracellular Ca2+ concentration on tight-junctional permeability in rat liver was studied by using the calcium ionophore A23187. Infusion of 100 microliters of dimethyl sulphoxide containing various amounts of A23187 over 30 min into isolated perfused livers was followed by a pulse of horseradish peroxidase (HRP) under single-pass conditions. The first biliary HRP peak, a measure of junctional permeability, was increased 4-fold with 100 micrograms of A23187. There were, however, no significant effects on bile flow or on aspartate aminotransferase leakage as compared with the control at this dosage, and thus the increase in junctional permeability was occurring without evidence of appreciable cholestatic or hepatocellular damage. Higher dosages of A23187, however, caused not only an increase in HRP peak height but also changes in bile flow and increases in aminotransferase leakage, indicating more extensive effects at these higher dosages. A second peak of HRP secretion, occurring 20-25 min after the HRP pulse, was also elevated approx. 3.5-fold; this may indicate that pinocytosis and transcellular movement of HRP are also increased under these conditions.

| S-EPMC1135521 | biostudies-other

Transcription profiling of human B lymphocytes from Scott syndrome patient and daughter, treated with the A23187 calcium ionophore

Project description:B lymphoblast samples from control individual, Scott syndrome patient and Scott syndrome daughter. From each samples one part was treated with A23187 ca2+ ionophore. Treated and non-treated samples were then cultured further. Each sample was then processed in duplicate for hybridization on the microarray

2007-07-19 | E-GEOD-1028 | biostudies-arrayexpress

Effects of calcium ions and the bivalent cation ionophore A23187 on the agglutination and fusion of chicken erythrocytes by Sendai virus.

Project description:1. Ca2+ (0.4-16 mM) had no detectable action on the agglutination of hen erythrocytes by Sendai virus. 2. Pretreatment of the cells with Ca2+ (0.1-8 mM) in the presence of the bivalent cation ionophore A23187 led, however, to a significant decrease in the subsequent agglutination of the cells by the virus. 3. It thus appears that the entry of Ca2+ into the interior of these cells decreases cellular agglutination by Sendai virus; possible interpretations of this phenomenon are discussed in terms of the movement of intramembranous particles. 4. With a small number of virions, maximum cell fusion by Sendai virus occurred in the presence of EGTA [ethanedioxybis(ethylamine)tetra-acetate]. 5. Virus-induced cell fusion was significantly decreased by Ca2+, even at a concentration of 0.2 mM; it is suggested that this may result from diminished interactions between virus particles and erythrocyte membranes.

| S-EPMC1163947 | biostudies-other

Ionophore A23187 induces a refractory state in thrombin-activated release of inositol phosphates.

Project description:The phosphatidylinositol cycle has been proposed to be involved in the regulation of platelet functionality through the control of cytoplasmic Ca2+ levels. However, the requirements of phospholipase C for Ca2+ has not yet been elucidated in intact platelets. The primary purpose of the present study was to investigate the Ca2+ requirements of this enzyme in platelets from miniature swine by taking advantage of the permeabilizing properties of the ionophore A23187. Our results strongly suggest that the treatment of platelets with A23187 induces a refractory state in thrombin-stimulated release of inositol phosphates while 5-hydroxytryptamine (serotonin)-secretory capacity in response to thrombin remained constant. This refractory state seems to be dependent on some cytochalasin-inhibitable cytoskeletal phenomena.

| S-EPMC1147195 | biostudies-other

Activation of (arachidonyl) phosphatidylinositol turnover in rabbit neutrophils by the calcium ionophore A23187.

Project description:The addition of the Ca2+ ionophore A23187 to rabbit neutrophils stimulated [14C]arachidonic acid incorporation into phosphatidylinositol and lysosomal enzyme secretion. A significant increase in phosphatidylinositol labelling was observed after a 2 min exposure to 0.1 microM-ionophore A23187. Maximum increases in rate of labelling were obtained with 1 microM-ionophore A23187 within 1 min, declining to basal rates after 15 min. Similarly, maximum rate of enzyme release occurred during the first 2 min of exposure to ionophore and release was essentially complete by 15 min. Threshold and peak ionophore A23187 concentrations for stimulating both processes were identical. In contrast with the specificity of phosphatidylinositol labelling induced by 1 microM-ionophore A23187 in the absence of cytochalasin B, ionophore also significantly stimulated labelling of phosphatidylserine and phosphatidylethanolamine in the presence of cytochalasin B. With a threshold ionophore concentration (0.1 microM), the enhanced incorporation of arachidonate was relatively specific for phosphatidylinositol in cytochalasin-treated cells. Ionophore A23187 did not accelerate labelling of phosphatidylinositol by [14C]acetate or [14C]glycerol, indicating that ionophore A23187 does not stimulate phosphatidylinositol synthesis de novo, although it did promote [14C]palmitate and [32P]Pi incorporation into neutrophil phosphatidylinositol. However, the increase in phosphatidylinositol labelling with these latter precursors was generally slower in onset and much more modest in magnitude than that observed with arachidonic acid. These results support the hypothesis that a Ca2+-dependent phospholipase, which acts on the arachidonate moiety of phosphatidylinositol, is responsible for initiating at least certain of the membrane events coupled to the release of secretory product from the neutrophil.

| S-EPMC1162774 | biostudies-other

The effects of the calcium ionophore, A23187, on the axoplasmic transport of dopamine beta-hydroxylase.

Project description:1 The effects of the ionophore, A23187, on the intra-axonal transport of dopamine beta-hydroxylase (DBH) were investigated in the cat hypogastric nerve-inferior mesenteric ganglion preparation by monitoring, in vitro, the enzyme accumulation above a ligature, 2 to 2.5 cm distal to the ganglion. 2 DBH accumulation in the proximal segment immediately above the ligature (P1) increased linearly up to 6 h, during incubation in normal Krebs solution at 37 degrees C. The ionophore, A23187, interfered with the enzyme accumulation, but did not modify the previously accumulated DBH activity present in P1. 3 The blocking effects of A23187 on DBH transport were greatly impaired in the absence of extracellular calcium ions; an excess of calcium in the bathing solution (7.5 mM) itself blocked the enzyme transport by 50%. 4 A23187 did not significantly modify the levels of adenosine triphosphate (ATP) in the segments P1 and P2 of the nerve proximal to the ligature. 5 Nerves incubated in an A23187-containing medium showed many mitochondria of normal shape and fine structure; however, typical microtubules or filaments were not seen in these preparations. 6 The results suggest that the ionophore A23187, by considerably raising the axoplasmic ionized calcium levels, interferes with the assembling of microtubules. In this manner, the ionophore would inhibit the transport of adrenergic vesicles and therefore of DBH along the axon. The results also provide additional evidence in favour of the view that for the transport system to work adequately, it is necessary to maintain the intra-axoplasmic ionized calcium concentration between certain critical levels.

| S-EPMC2044350 | biostudies-other

Biosynthesis of platelet-activating factor by cultured rat Kupffer cells stimulated with calcium ionophore A23187.

Project description:Cultured rat Kupffer cells synthesize and release platelet-activating factor (PAF) when stimulated with calcium ionophore A23187. The production of PAF is concentration- and time-dependent and, based upon [3H]serotonin release assays, approx. 1.0 pmol of PAF is formed per 8 x 10(6) cells during 10 min of ionophore stimulation. It is suggested that Kupffer cells are important cellular components which produce and release PAF in order to facilitate communication between hepatic sinusoidal and parenchymal cells. Further, it is suggested that such mediator production in response to reticulo-endothelial cell stimulation causes the hepatic glycogenolytic response previously in the isolated perfused rat liver.

| S-EPMC1135662 | biostudies-other

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