scholarly journals Role of calcium ions in the control of embryogenesis of Xenopus. Changes in the subcellular distribution of calcium in early cleavage embryos after treatment with the ionophore A23187.

1979 ◽  
Vol 80 (3) ◽  
pp. 589-604 ◽  
Author(s):  
J C Osborn ◽  
C J Duncan ◽  
J L Smith
Keyword(s):  
Divalent Cations ◽  
Subsequent Development ◽  
Abnormal Development ◽  
Ionophore A23187 ◽  
Early Cleavage ◽  
Amphibian Embryo ◽  
High Incidence ◽  
Intracellular Action

Treatment of stage 5 Xenopus embryos with the ionophore A23187 for only 10 min, in the absence of extracellular Mg2+ and Ca2+, causes cortical contractions and a high incidence of abnormal embryos during subsequent development. Cation analysis shows that divalent ions are not lost from the embryos, but that Ca2+ is redistributed within the subcellular fractions. Ca2+ is probably released from yolk platelets and/or pigment granules by the action of A23187, [Ca2+] rises in the cytosol, and the mitochondria attempt to take up this free Ca2+. The mitochondria concomitantly undergo characteristic ultrastructural transformations, changing towards energized-twisted and energized-zigzag conformations. A23187 allows these changes to be demonstrated in situ. Extracellular divalent cations (10(-4) M) interfere with this intracellular action of A23187. Intracellular accumulation of Na+ (by treatment with ouabain) or Li+ also causes abnormal development, probably by promoting a release of Ca2+ from the mitochondria. It is suggested (a) that all these treatments cause a rise in [Ca2+]i which interferes with normal, integrated cell division, so causing, in turn, abnormal embryogenesis, (b) that levels of [Ca2+]i are of importance in regulating cleavage, (c) that the mitochondria could well have a function in regulating [Ca2+]i during embryogenesis in Xenopus, and (d) that vegetalizing agents may well act by promoting a rise in [Ca2+]i in specific cells in the amphibian embryo.

Cholinergic regulation of guinea pig duodenal bicarbonate secretion

1993 ◽  
Vol 265 (2) ◽  
pp. G270-G276 ◽  
Author(s):  
H. S. Odes ◽  
R. Muallem ◽  
R. Reimer ◽  
W. Beil ◽  
M. Schwenk ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Vagal Stimulation ◽  
Ionophore A23187 ◽  
Loop Model ◽  
Cholinergic Regulation ◽  
Intracellular Signals ◽  
Duodenal Bicarbonate Secretion ◽  
Series Of Experiments

Although it is well known that vagal stimulation induces duodenal HCO3- secretion, there is presently no information about the nature of the cholinoceptor and the intracellular signals involved. In a series of experiments performed in a guinea pig duodenal loop model in situ, intravenous carbachol, atropine, pirenzepine, and hexamethonium were used to determine the extent of cholinergic stimulation and the types of cholinoceptors. Carbachol (2 micrograms.kg-1.5 min-1) stimulated HCO3- secretion threefold, and atropine (0.1 mg.kg-1.5 min-1) and pirenzepine (1 mg.kg-1.5 min-1) both abolished this effect. In addition, hexamethonium (0.3 mg.kg-1.5 min-1) inhibited carbachol-stimulated duodenal HCO3- secretion. Vasoactive intestinal peptide (VIP, 5 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, and this action was partly inhibited by atropine (0.1 mg.kg-1.5 min-1) but not by pirenzepine (1 mg.kg-1.5 min-1). [4Cl-D-Phe6,Leu17]VIP (3.3 mg/kg), an antagonist to VIP, reduced basal, VIP-stimulated, and carbachol-stimulated HCO3- secretion. To examine the role of Ca2+ in this process, Ca2+ ionophore A23187, verapamil, and nifedipine were employed. A23187 (5, 50, 500 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, an effect blocked by the VIP antagonist, and modestly augmented the effect of carbachol. Verapamil (0.2 mg.kg-1.5 min-1) and nifedipine (1.7 mg.kg-1.5 min-1) stopped the effect of carbachol on duodenal HCO3- secretion. These results suggest, that in cholinergic regulation of duodenal HCO3- secretion, the M-cholinoceptor pathway, Ca2+, and VIP are involved.

scholarly journals The role of divalent cations in the regulation of microtubule assembly. In vivo studies on microtubules of the heliozoan axopodium using the ionophore A23187.

1976 ◽  
Vol 70 (3) ◽  
pp. 527-540 ◽  
Author(s):  
M Schliwa
Keyword(s):  
Divalent Cations ◽  
Light And Electron Microscopy ◽  
Microtubule Assembly ◽  
In Vivo Studies ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Microtubule Formation

Low concentrations of calcium and magnesium ions have been shown to influence microtubule assembly in vitro. To test whether these cations also have an effect on microtubules in vivo, specimens of Actinosphaerium eichhorni were exposed to different concentrations of Ca++ and Mg++ and the divalent cation ionophore A23187. Experimental degradation and reformation of axopodia were studied by light and electron microscopy. In the presence of Ca++ and the ionophore axopodia gradually shorten, the rate of shortening depending on the concentrations of Ca++ and the ionophore used. Retraction of axopodia was observed with a concentration of Ca++ as low as 0.01 mM. After transfer to a Ca++-free solution containing EGTA, axopodia re-extend; the initial length is reached after about 2 h. Likewise, reformation of axopodia of cold-treated organisms is observed only in solutions of EGTA or Mg++, whereas it is completely inhibited in a Ca++ solution. Electron microscope studies demonstrate degradation of the axonemal microtubular array in organisms treated with Ca++ and A23187. No alteration was observed in organisms treated with Mg++ or EGTA plus ionophore. The results suggest that, in the presence of the ionophore, formation of axonemal microtubules can be regulated by varying the Ca++ concentration in the medium. Since A23187 tends to equilibrate the concentrations of divalent cations between external medium and cell interior, it is likely that microtubule formation invivo is influenced by micromolar concentrations of Ca++. These concentrations are low enough to be of physiological significance for a role in the regulation of microtubule assembly in vivo.

scholarly journals Regulation of macrophage lysosomal enzyme secretion: role of arachidonate metabolites, divalent cations and cyclic AMP

1980 ◽  
Vol 44 (1) ◽  
pp. 299-315
Author(s):  
R.M. McMillan ◽  
D.E. Macintyre ◽  
J.E. Beesley ◽  
J.L. Gordon
Keyword(s):  
Cyclic Amp ◽  
Lysosomal Enzyme ◽  
Lysosomal Enzymes ◽  
Divalent Cations ◽  
Cell Types ◽  
Enzyme Secretion ◽  
Ionophore A23187 ◽  
Enzyme Release ◽  
Arachidonate Metabolites

We have investigated the role in macrophage lysosomal enzyme release of arachidonate metabolites, extracellular divalent cations and cyclic AMP (cAMP) which modulate secretion in other cell types. Lysosomal enzyme secretion induced by zymosan was accompanied by release of malondialdehyde (MDA), which is derived from arachidonic acid via prostaglandin synthase. Blockade of MDA formation, by aspirin or indomethacin, was associated with only a small inhibitory effect on lysosomal enzyme release by zymosan: arachidonate metabolites thus play only a minor role in mediating macrophage lysosomal enzyme release. Zymosan-induced secretion of lysosomal enzymes from macrophages did not require extracellular magnesium or calcium although release was enhanced by magnesium and inhibited by calcium. These effects may be related to an influence of the ions on phagocytosis. Elevation of intracellular divalent cation concentrations, by ionophore A23187, induced release of lysosomal enzymes but this was a result of cell lysis. Adenylate cyclase stimulants and dibutyryl cAMP produced slight inhibition of zymosan-induced lysosomal enzyme release. Aminophylline and papaverine caused more marked inhibition but their effects may be due to actions independent of phosphodiesterase inhibition. Our data indicate that arachidonate metabolites and cAMP do not play a major role in regulating zymosan-induced enzyme release from macrophages. Extracellular calcium and magnesium may modulate secretion but the role of intracellular divalent cations remains to be established. We conclude that macrophage lysosomal enzyme secretion is controlled by regulatory mechanisms different from those which control similar degranulation processes in other cell types.

scholarly journals Evidence for a role of glycoprotein IIb-IIIa, distinct from its ability to support aggregation, in platelet activation by ionophores in the presence of extracellular divalent cations

Blood ◽  
1994 ◽  
Vol 83 (9) ◽  
pp. 2549-2559 ◽  
Author(s):  
B Lages ◽  
HJ Weiss
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Divalent Cations ◽  
Ionophore A23187 ◽  
Myristate Acetate ◽  
Serotonin Secretion ◽  
Occupied State ◽  
Induced Aggregation

Abstract Ionophore A23187-induced 14C-serotonin secretion and thromboxane B2(TxB2) formation were found to be absent in citrated platelet-rich plasma (PRP) from thrombasthenic subjects and in normal PRP treated with glycoprotein (GP) IIb-IIIa complex-specific monoclonal antibodies. Both responses were restored to normal levels when 5 mmol/L EDTA was present, indicating that their absence was not caused by the absence of aggregation per se. In gel-filtered platelets (GFP) incubated with various additions, the blockade or absence of GPIIb-IIIa resulted in reduced A23187-induced secretion and TxB2 formation in media containing 1 mmol/L Ca2+ with or without fibrinogen and 1 mmol/L Mg2+ plus fibrinogen, but not when Ca, Mg-free buffer alone, 1 mmol/L EDTA, or fibrinogen alone were present. In contrast, no such dependence or GPIIb- IIIa was seen in GFP stimulated with thrombin or phorbol myristate acetate in the presence of 1 mmol/L Ca2+, 1 mmol/L EDTA, or buffer alone. The inhibition of ionophore-induced responses seen in both normal GFP treated with antibodies and thrombasthenic GFP was not associated with any significant alteration of the ionophore-mediated [Ca2+]i increase, as measured in both aequorin-loaded GFP stimulated with A23187 and fura-2-loaded GFP stimulated with ionomycin. Incubation of normal GFP with either the monoclonal antibodies or the ligand binding site peptide RGDS in the presence of 1 mmol/L Ca2+ caused virtually complete inhibition of A23187-induced aggregation, measured as the loss of single platelets, but RGDS, in contrast to the antibodies, did not inhibit secretion or TxB2 formation. We conclude that platelet activation induced by ionophores in the presence, but not in the absence, of extracellular divalent cations involves a GPIIb-IIIa- dependent process that most likely involves a property of the ligand- occupied form of the complex distinct from its ability to support aggregation. This could represent another example of an aggregation- independent activity of the receptor-occupied state of the GPIIb-IIIa complex in signal transduction.

Parthenogenetic development of mouse embryos in vivo

Development ◽  
1973 ◽  
Vol 30 (3) ◽  
pp. 519-545
Author(s):  
Anna Witkowska
Keyword(s):  
Polar Body ◽  
Subsequent Development ◽  
Hormonal Treatment ◽  
Inbred Strains ◽  
Early Cleavage ◽  
Parthenogenetic Development ◽  
Second Polar Body ◽  
First Time

Newly ovulated eggs from CBA-p and CBA-T6T6 inbred strains were activated in situ with an electric shock of 20–50 V. Both spontaneously ovulating females mated with vasectomized males (strain A) and those induced to ovulate and kept apart from males were used. The immediate reaction of eggs was examined 5–7 h after activation and their subsequent development was followed every day up to the 6th day (eggs examined on the 5th and 6th day were tube-locked by a ligature). In spontaneous ovulators the highest yield of activated eggs was obtained following 30 V shock (75%), with a mean for four series (20, 30, 40 and 50 V) of 46·1%. The most common reaction is extrusion of the second polar body (2 PB) and formation of one pronucleus (about 70% of activated eggs). Other types of reaction include: immediate cleavage, suppression of 2 PB with formation of two or, very rarely, one pronucleus. Thus the majority of eggs are potentially haploid. No relationship between the frequency of various types of reaction and the strength of the shock (voltage) was observed. Up to the 3rd day cleavage proceeds at a normal rate and appears to slow down during the 4th day. In spontaneously ovulating females the incidence of blastocysts among developing eggs rises from 3·4% on the 4th day to 52·5% on the 5th day; the corresponding figures for induced ovulations are 10% and 23·6%. Some embryos despite being composed of a large number of cells (40–120) do not undergo cavitation and remain morulae. On the basis of karyological examination of 60 embryos with analysable metaphase plates 60% were classified as haploid, 16·7% as diploid, 1·7% as tetraploid and 21·6% as haploid/diploid mosaics. During early cleavage binucleate blastomeres (a presumed step in regulation from n to 2n) were observed only in eggs from induced ovulations. In embryos developed from spontaneously ovulated eggs n/2n mosaics were observed for the first time on the 5th day. In general, spontaneously ovulated eggs developed better after activation (both in quantitative and qualitative terms) than those obtained following hormonal treatment.

Calcium and wound healing in Xenopus early embryos

Development ◽  
1982 ◽  
Vol 67 (1) ◽  
pp. 195-205
Author(s):  
Martin Stanisstreet
Keyword(s):  
Wound Healing ◽  
Divalent Cations ◽  
Local Application ◽  
Ionophore A23187 ◽  
Excess Calcium ◽  
Early Embryos ◽  
Cell Shapes ◽  
Healing Of Wounds ◽  
Made In

The role of calcium in the healing of wounds made in the ectoderm of Xenopus neurulae has been studied. Embryos have been wounded in the presence of calcium inhibitors, and the effects on wound healing observed by scanning electron microscopy. In addition, unwounded embryos have been exposed to a local application of ionophore A23187 to simulate the possible calcium fluxes following wounding. Lanthanum, which competes for calcium channels, inhibits wound healing. EDTA, which binds divalent cations, also inhibits wound healing, but its effect can be reversed by the addition of excess calcium. Local application of ionophore A23187, which promotes transport of calcium across biological membranes, results in a local change in cell shapes. These observations lend support to the hypothesis that wound healing in amphibian early embryos, which is effected by changes in cell shapes similar to those seen in certain examples of normal morphogenesis, is initiated by a local influx of calcium into cells.

scholarly journals Evidence for a role of glycoprotein IIb-IIIa, distinct from its ability to support aggregation, in platelet activation by ionophores in the presence of extracellular divalent cations

Blood ◽  
1994 ◽  
Vol 83 (9) ◽  
pp. 2549-2559 ◽  
Author(s):  
B Lages ◽  
HJ Weiss
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Divalent Cations ◽  
Ionophore A23187 ◽  
Myristate Acetate ◽  
Serotonin Secretion ◽  
Occupied State ◽  
Induced Aggregation

Ionophore A23187-induced 14C-serotonin secretion and thromboxane B2(TxB2) formation were found to be absent in citrated platelet-rich plasma (PRP) from thrombasthenic subjects and in normal PRP treated with glycoprotein (GP) IIb-IIIa complex-specific monoclonal antibodies. Both responses were restored to normal levels when 5 mmol/L EDTA was present, indicating that their absence was not caused by the absence of aggregation per se. In gel-filtered platelets (GFP) incubated with various additions, the blockade or absence of GPIIb-IIIa resulted in reduced A23187-induced secretion and TxB2 formation in media containing 1 mmol/L Ca2+ with or without fibrinogen and 1 mmol/L Mg2+ plus fibrinogen, but not when Ca, Mg-free buffer alone, 1 mmol/L EDTA, or fibrinogen alone were present. In contrast, no such dependence or GPIIb- IIIa was seen in GFP stimulated with thrombin or phorbol myristate acetate in the presence of 1 mmol/L Ca2+, 1 mmol/L EDTA, or buffer alone. The inhibition of ionophore-induced responses seen in both normal GFP treated with antibodies and thrombasthenic GFP was not associated with any significant alteration of the ionophore-mediated [Ca2+]i increase, as measured in both aequorin-loaded GFP stimulated with A23187 and fura-2-loaded GFP stimulated with ionomycin. Incubation of normal GFP with either the monoclonal antibodies or the ligand binding site peptide RGDS in the presence of 1 mmol/L Ca2+ caused virtually complete inhibition of A23187-induced aggregation, measured as the loss of single platelets, but RGDS, in contrast to the antibodies, did not inhibit secretion or TxB2 formation. We conclude that platelet activation induced by ionophores in the presence, but not in the absence, of extracellular divalent cations involves a GPIIb-IIIa- dependent process that most likely involves a property of the ligand- occupied form of the complex distinct from its ability to support aggregation. This could represent another example of an aggregation- independent activity of the receptor-occupied state of the GPIIb-IIIa complex in signal transduction.

Testosterone Potentiation of Ionophore and ADP Induced Platelet Aggregation : Relationship to Arachidonic Acid Metabolism

1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Unsaturated Fatty Acids ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Induced Aggregation

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.

THE ROLE OF SHAIKH NURIDDIN AND SHOKHMALIK IN THE POLITICAL PROCESSESTHAT TOOK PLACE IN THE FIRST DAYS AFTER THE DEATH OF AMIR TEMUR

2020 ◽  
Vol 11 (3) ◽  
pp. 47-54
Author(s):  
Laylo Begimkulova ◽  
Keyword(s):  
Subsequent Development ◽  
Primary Sources ◽  
The Political ◽  
Political Processes

In this article, the author, on the basis of historical primary sources, highlights the role and influence of the great emirs Shaikh Nuriddin and Shokhmalik on the political processes that took place after the death of Amir Temur and the subsequent development of events.

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