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Results for “Calcimycin”

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At least 19 recordsLinked to original sources
PubMed1992

Inhibition of calcimycin-induced stimulation of cytosolic calcium in human PMN by a LTB4 receptor antagonist.

This study investigates the significance of PMN-derived LTB4 for PMN activation by using a selective LTB4 antagonist (SC 41930). Human PMN were stimulated by platelet-activating-factor (PAF, 3 microM), a receptor dependent agonist, or by calcimycin (A 23187, 10 microM), a receptor independent agonist. PMN activation was determined by LTB4 release and changes in free cytosolic Ca++ levels. Pretreatment of the PMN with SC 41930 (0.1-10 microM) caused a concentration-dependent inhibition of agonist induced rise in cytosolic Ca++ with both PAF and calcimycin. Interestingly, at the same concentrations of SC 41.930, there was a concentration-dependent inhibition of LTB4 release. Control experiments with a cell-free 5-lipoxygenase preparation did not show any direct effect of SC 41930 on the enzyme under conditions when nordihydroguiaretic acid was active. The data demonstrate a nonselective inhibition of agonist induced PMN activation by the LTB4 receptor antagonist SC 41930 and suggest that formation of endogenous LTB4 is involved in a positive feed-back loop that is required for maximum stimulation of PMN function even by a calcium ionophore.

Arachidonate 5-Lipoxygenase↗
PubMed1992

Inhibitory effects of tetrandrine on Bay k 8644-stimulated contraction of isolated rabbit aortic strips.

In the presence of KCl 19 mmol.L-1, calcium agonist Bay k 8644 0.47 mumol.L-1 elicited a strong contraction of isolated rabbit aortic strips, and this contraction was concentration-dependently inhibited by tetrandrine; but this antagonism was noncompetitive. Calcium ionophore calcimycin evoked contraction was markedly depressed by tetrandrine. The results suggested that tetrandrine might not only inhibit transmembrane influx of calcium via potential-dependent channels but also interfere with other processes related to calcium.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1977

Granule release by polymorphonuclear leukocytes treated with the ionophore A23187.

Polymorphonuclear leukocytes (PMN's) incubate three to eight minutes at 37 degrees C in medium containing 1 X 10(-6) M of the ionophore antibiotic A23187 released their cytoplasmic granules into the extracellular medium. Transmission electron microscopy of treated cells showed microfilament bundles extending between adjacent granules within the cytoplasm and between granules and the plasma membrane. Tiny dense projections (beads) 8-12 nm in diameter were observed along segments of the cytoplasmic surface of the plasma membrane with a periodicity of 20-30 nm. These beads were observed on the plasma membrane only in the vicinity of intra- or extracytoplasmic granules. The structural relationships of the beads with the plasma membrane microfilaments suggest they play a role in the process of ionophore-induced granule release from polymorphonuclear leukocytes.

Animals↗
PubMed1979

Induction of exocytosis from glomus cells by incubation of the carotid body of the rat with calcium and ionophore A23187.

Carotid bodies from adult rats were electron microscopically studied after incubation in glucose-containing salt solutions containing calcium and/or ionophore A23187 or neither. In the absence of the ionophore, adding or omitting calcium had no effect on the fine structure of the glomus cells. Incubation in the medium containing both 1 mM calcium and the ionophore caused the appearance of exocytotic membrane profiles in several glomus cells. Exocytosis was not seen when only A23187 and endogenous calcium was present. For exocytosis to occur, calcium appeared to be essential and the event seemed to be due to a rise in the intracellular calcium concentration caused by the ionophore.

Animals↗
PubMed1978

Decreased lymphocyte response to PHA, Con-A, and calcium ionophore (A23187) in patients with RA and SLE, and reversal with levamisole in rheumatoid arthritis.

The mechanism of poor lymphocyte transformation to mitogens was studied in selected patients with rheumatoid arthritis and systemic lupus erythematosus. Low lymphocyte response to PHA and Con-A in media containing autologous and homologous sera was usually associated with poor response to the calcium ionophore A23187, which induces blastogenesis by a different mechanism. The low lymphocyte response to mitogens in patients with rheumatoid arthritis could be restored by in vivo treatment with the anthelmintic drug, levamisole. The present findings suggest that intrinsic defects are responsible for the decreased cellular response in patients with rheumatoid arthritis and systemic lupus erythematosus.

Adolescent↗
PubMed1978

Generation and release of eosinophil chemotactic factor from human polymorphonuclear neutrophils by arachidonic acid.

This study describes the generation and release of an eosinophil chemotactic factor from human polymorphonuclear neutrophils, rat basophilic leukemia cells, and from a lymphocyte monocyte basophil suspension by arachidonic acid (AA). The eosinophil chemotactic factor (ECF) is highly specific for eosinophils and resembles the ECF activity obtained from human polymorphonuclear neutrophils after stimulation with the Ca ionophore or during phagocytosis. In this regard, AA-induced ECF represents a biological activity distinct from oxidized AA and its conversion products. AA may therefore have a dual function: it represents an important mechanism of cell activation; as AA is converted into prostaglandins, it appears likely that they exert a modulatory and a suppressive role on biological functions, such as chemotaxis and phagocytosis.

Animals↗
PubMed1978

Chemiluminescence and immune cell activation. I. Early activation of rat thymocytes can be monitored by chemiluminescence measurements.

Immediately after the addition of concanavalin A, rat thymocytes respond, in the presence of luminol, with a burst of chemiluminescence (CL) that can be conveniently monitored in an ordinary liquid scintillation spectrometer. Peak CL is reached after 50 sec. Addition of catalase suppresses 65% of the CL, suggesting that H2O2 generation may be its major source. CL with different kinetic characteristics can also be generated by the calcium ionophore A23187. Our rat thymocytes contain approximately 0.1% endogenous macrophages. Bone marrow-derived rat macrophages also respond to concanavalin A or A23187 stimulation with a burst of CL. However, the kinetic properties of CL as well as the inhibition of CL by catalase in these cells differ markedly from those of thymocyte preparations, suggesting that the major portion of the CL in rat thymocytes actually originates in T lymphocytes. Because CL measurements allow the monitoring of very early events in cell activation and because of the simplicity of the technique, CL measurements may become a useful method for the study of lymphocyte activation, of macrophage-lymphocyte interactions, as well as for the rapid screening for specificity and reactivity of T lymphocyte populations.

Animals↗
PubMed1979

Platelet-activating factor and macrophages. I. Evidence for the release from rat and mouse peritoneal macrophages and not from mastocytes.

Platelet-activating factor (PAF) is a phospholipid mediator of anaphylaxis, released from basophils of several mammalian species, that aggregates platelets and releases their vasoactive amines. The ionophore A23 187 induced the release of PAF from rat and mouse peritoneal cells, a mixed cell population that was fractionated using 5--15% Ficoll gradients and adherence to plastic petri dishes. PAF was associated with large, acid phosphatase-containing, adherent mononuclear cells. Mastocytes did not release PAF but released histamine by the action of ionophore or 48/80; they could not be held responsible for inactivation of PAF or inhibition of the PAF-induced platelet aggregation. These data indicate that, besides blood basophils, peritoneal macrophages are a likely source for PAF, a result that adds a new important function to the macrophage:aggregation of platelets and liberation of their inflammatory and vasoactive substances.

Animals↗
PubMed1978

Altered membrane-associated functions in chronic lymphocytic leukemia cells.

Peripheral blood lymphocytes consisting mainly of neoplastic B cells from patients with chronic lymphocytic leukemia (CLL cells) showed a markedly reduced response to the human B-cell mitogens anti-beta2 microglobulin, Sepharose-bound protein A and Sepharose-bound anti-human immunoglobulin (anti F(ab')2) in all of nine patients studied. On the other hand, CLL cells from three out of eight patients tested responded well to the calcium ionophore A23187. Sepharose-bound protein A and anti-beta2 microglobulin also failed to induce increased uptake of 86Rubidium (potassium analogue) in CLL cells as compared to B-cell-enriched preparations of normal peripheral blood lymphocytes. The capacity of CLL cells to cap various surface markers including beta2 microglobulin was reduced. On the other hand, surface concentrations of beta2 microglobulin were not reduced as measured by fluorescein-labelled anti-beta2-microglobulin in single-cell cytofluorometry. It is concluded that various membrane-associated events elicited by ligand-receptor interactions are altered or blocked in CLL cells.

Aged↗
PubMed1992

Protein kinase C involved in zymosan-induced release of arachidonic acid and superoxide but not in calcium ionophore-elicited arachidonic acid release or formation of prostaglandin E2 from added arachidonate.

Zymosan and phorbol ester induced in liver macrophages the release of arachidonic acid, prostaglandin E2, and superoxide; the calcium ionophore A 23187 elicited a release of arachidonic acid and prostaglandin E2 but not of superoxide, and exogenously added arachidonic acid led to the formation of prostaglandin E2 only. The zymosan- and phorbol-ester-induced release of arachidonic acid, prostaglandin E2, and superoxide was dose-dependently inhibited by staurosporine and K252a, two inhibitors of protein kinase C, and by pretreatment of the cells with phorbol ester which desensitized protein kinase C. The release of arachidonic acid or prostaglandin E2 following the addition of A 23187 or arachidonic acid was not affected by these treatments. Zymosan and phorbol ester but not A 23187 or arachidonic acid induced a translocation of protein kinase C from the cytosol to membranes in intact cells. These results demonstrate an involvement of protein kinase C in the zymosan- and phorbol-ester-induced release of arachidonic acid, prostaglandin E2, and superoxide; the release of arachidonic acid and prostaglandin E2 elicited by A 23187 and the formation of prostaglandin E2 from exogenously added arachidonic acid, however, is independent of an activation of protein kinase C.

Alkaloids↗
PubMed1975

Spontaneous and induced membrane hyperpolarizations in macrophages.

The electrophysiological properties of guinea pig peritoneal macrophages cultured in vitro were studied using standard intracellular recording techniques. The mean transmembrane potential, input resistance and time constant recorded from these cells were -13.1 mV, 143 Mohms, and 18 msec respectively. The majority of macrophages exhibited spontaneous hyperpolarizations (HA) of 4-8 seconds in duration and 10-50 mV in amplitude. Mouse peritoneal macrophages and human monocyte-derived macrophages manifested similar HA. HA could be induced by either mechanical stimulation or application of hyperpolarizing currents of 2-8 namps. HA had a mean reversal potential of -53 mV. Increasing the extracellular [K+] 10-fold resulted in a 50 mV shift in reversal potential. Addition of EGTA (1.5 mM) inhibited both spontaneous and evoked macrophage HA in the presence of excess Mg++. The divalent cation ionophore, A23187 induced prolongation of HA at low concentration (0.6 X 10(-6) M) and resulted in sustained hyperpolarization at higher concentration (2.0 X 10(-6) M). Addition to EGTA to cells treated with A23187 abolished HA. These data indicate that: (1) cultured macrophages from a variety of species exhibit spontaneous and induced HA, (2) development of HA is related to an increase in membrane permeability to K+, and (3) Ca++ may regulate the spontaneous and evoked electrical activity of the macrophage membrane presumably by affecting K+ permeability.

Animals↗
PubMed1976

The role of calcium in the inhibition of cAMP accumulation in epiphyseal cartilage cells exposed to physiological pressure.

A hydrostatic pressure of 60g/cm sq (0.85 psi) inhibits the accumulation of cAMP in cells isolated from the proliferative zone of chick-tibia epiphyseal cartilage. The following findings indicate that this effect is mediated by a translocation of calcium: (i) the pressure enhances the cellular uptake of radiocalcium; (ii) the pressure effect on cAMP can be simulated by the calcium-ionophore A23187; (iii) the effects of pressure and A23187 are non-additive; (iv) the pressure effect is not produced in the presence of ethylenebis-(oxyethylenenitrilo)-pressure effect is not produced in the presence of ethylenebis-(oxyethylenenitrilo)-tetraacetic-acid (EGTA); (v) the particulate adenyl cyclase activity of the proliferative zone is susceptible to non-competitive calcium inhibition. Throughout this study cells from the hypertrophic zone of the same epiphyses were used as controls. In these cells the calcium uptake was enhanced by pressure, but the cAMP level was not affected by pressure, A23187 or EGTA. This change in responsiveness, which accompanies the maturation of the cartilage cells, was shown to be due to a decrease in the calcium-inhibition of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1978

On the stimulation of rat thymocyte 3-O-methyl-glucose transport by mitogenic stimuli.

Pretreatment of rat thymus lymphocytes with N-ethyl-maleimide prevents the stimulation of 3-O-methyl-glucose transport by concanavalin A or ionophore A23187 but does not affect the ability of concanavalin A to induce a rapid increase in cellular Ca2+take. N-ethyl-maleikide added after concanavalin A amplifies rather than prevents the subsequent stimulation of 3-O-methyl-glucose transport. Incubation of thymocytes with concanavalin A produces a decrease of 43% in the apparent Ki for phloretin, a competitive inhibitor of 3-O-methyl-glucose transport, without affecting the apparent Km for the substrate. Similarly, very low concentrations of cytochalasin B inhibit concanavalin A-stimulated glucose transport preferentially, without markedly affecting the unstimulated transport rates. The similarity between concanavalin A-stimulated 3-O-methyl-glucose transport in thymocytes and insulin-stimulated glucose transport in adipose tissue, with particular emphasis on the effects of the modifying agents described in this paper, is discussed.

Animals↗
PubMed1979

A calcium requirement for movement of cultured cells.

When calcium is removed from culture medium, motility of cultured cells is decreased. The effect is rapid, reversible and pronounced. Decreased motility is observed with normal mouse Balb/c 3T3 cells, mouse L929 cells, rat kidney fibroblasts and chick embryo fibroblasts. The calcium dependence of movement can be observed both with individual cells and with the movement of the margin of a monolayer into a wound. Magnesium will not substitute for calcium to maintain motility. Strontium will substitute, but is not as effective as calcium for maintaining cell movement. Low concentrations of the divalent cation ionophore A23187 (0.5-1 micron) partially reverse the reduced migration observed at low calcium concentrations. These results are consistent with the hypothesis that movement of non-muscle cells occurs through mechanisms similar to those important in the contraction of muscle.

Animals↗
PubMed1979

Rapid alterations in cellular morphology and plasma membrane structure induced in rat thymocytes by mitogenic stimuli.

Under conditions where a maximum stimulation of 3-O-methyl-glucose transport is observed, three thymocyte mitogens (concanavalin A, ionophore A23187 and hydrogen peroxide) cause cell rounding and a decrease in the density of intra-membrane particles on the plasma membrane. The early effects of mitogens on the thymocyte plasma membrane are similar to those of osmotic shock.

Animals↗
PubMed1992

Reactive oxygen species and human spermatozoa: analysis of the cellular mechanisms involved in luminol- and lucigenin-dependent chemiluminescence.

We have shown that human spermatozoa generate and release reactive oxygen species that can be detected by chemiluminescence techniques. Analysis of the cellular mechanisms responsible for this activity suggests that the probe, luminol, undergoes an intracellular dioxygenation reaction mediated by hydrogen peroxide and a sperm peroxidase located within the acrosome. Support for this model included the following observations: (1) the luminol-dependent signal could be suppressed with peroxidase inhibitors, phenylhydrazine and sodium azide; (2) this suppression could be reversed by the addition of an azide-insensitive peroxidase, horse radish peroxidase (HRP); (3) inhibition of intracellular superoxide dismutase (SOD) with potassium cyanide (KCN) suppressed the luminol signal; (4) peroxidase activity could be detected in purified populations of human spermatozoa with 3,3',5,5' tetramethylbenzidine (TMB); (5) this peroxidase was active at the pH prevailing within the acrosomal vesicle; and (6) peroxidase activity and luminol-dependent chemiluminescence were minimal in spermatozoa exhibiting a congenital absence of acrosomes. Human spermatozoa could also generate lucigenin-dependent chemiluminescent signals that could neither be suppressed with peroxidase inhibitors nor enhanced by the addition of peroxidase. However, these signals could be enhanced by suppression of intracellular SOD with KCN or inhibited by exogenous SOD, suggesting that lucigenin was responding to superoxide anion released into the extracellular space. The ability of chemiluminescent techniques to detect and discriminate the production of superoxide and hydrogen peroxide by spermatozoa should facilitate the further analysis of reactive oxygen species as mediators of normal and abnormal human sperm function.

Acridines↗