Calcium signals and phospholipid methylation in eukaryotic cells

Moore, John P.; Johannsson, A.; Hesketh, T R; Smith, Gavin; Metcalfe, James C.

doi:10.1042/bj2210675

Cited by 42 publications

(19 citation statements)

References 59 publications

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“…In these experiments, the mast cell pool of S-adenosylmethionine was efficiently labelled. In our experience, and from the reported findings of Moore et al [13], incubation of rodent mast cells with 3H-methionine under basal and stimulated conditions results in at least 60% of the radiolabel being incorpo rated into the neutral lipid fraction and not phospho lipid. The reasons for the inability of research groups in the United Kingdom to reproduce the IgE-dependent phospholipid méthylation is unexplained at the present time.…”

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confidence: 52%

“…Firstly, on prelabeling ro dent and human mast cells with radiolabeled methio nine, there occurs a transient, incorporation of radiolabeled methyl groups into chloroform-extractable phospholipid which, by occurring 5-30 s following cell activation, precedes the onset of mediator secre tion. Secondly, synthetic analogues of adenosine such as 3-deazaadenosine (DZA) alone, or more effectively in the presence of exogenous homocysteine-thiolactone (which inhibit methyltransferase activity by increasing the intracellular concentrations of S-adenosylhomocysteine and its 3-deaza analogue), produce a concentration-related inhibition of IgE-dependent phospholipid méthylation, 45Ca++ flux and histamine secretion [12], However, over the last 2 years a number of workers have had difficulty in demonstrating the incorporation of radiolabeled methyl groups into phospholipids in experiments using purified rat mast cells activated for mediator secretion by an IgE-dependent mechanism [13,14], With the help of Dr. T. Ishizaka we have tried to reproduce the exact experi mental conditions under which phospholipid méthyl ation has been demonstrated. However, while IgE-dependent histamine secretion occurred in the range of 20-30%, we have been unable to demonstrate any specific incorporation of radiolabeled methyl groups from methionine into chloroform-extractable lipid.…”

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confidence: 99%

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Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

Holgate

Benyon

Howarth

et al. 1985

Int Arch Allergy Immunol

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There is now compelling evidence to incriminate bronchial mast cells in the pathogenesis of bronchoconstriction of allergic asthma. Human mast cells isolated from lung tissue or bronchoalveolar lavage release histamine and generate eicosanoids upon IgE-dependent activation. In this paper we present data that raise doubts about the significance of phospholipid methylation in IgE-dependent activation-secretion coupling and provide evidence that drugs such as 3-deazaadenosine inhibit mediator secretion by inhibiting phosphodiesterase, in addition to inhibiting putative methylation pathways. Activation of human mast cells and basophils also stimulates adenylate cyclase to increase levels of cyclic AMP, which, on the basis of pharmacological manipulation with purine nucleosides, we believe is involved in the progression of the secretory response. Human lung cells also generate both cyclo- and lipoxygenase products of arachidonate upon Ca⁺⁺-dependent stimulation with complex interactions occurring between these pathways in the presence of the leukotriene inhibitor, Piriprost. The role of mast cells in the immediate airway response to inhaled allergens in asthma was demonstrated by showing an interaction between nonspecific bronchial reactivity and mast cell reactivity in predicting the airway response upon antigen inhalation. Further confirmation of this concept was obtained by showing an inverse relationship between the release of histamine and neutrophil chemotactic factor (NCF) into the circulation induced by antigen challenge, and nonspecific airway reactivity. The identification of significant increases in circulating mediators following antigen provocation of patients with seasonal asthma enabled the effects of drugs used in the treatment of asthma to be compared on airway calibre and mast cell mediator release. Sodium cromoglycate partially inhibited the airway and plasma histamine responses with antigen, but totally inhibited the increases in NCF. Salbutamol completely inhibited all responses, while ipratropium bromide, which produced the same bronchoconstriction as achieved with salbutamol, had no effect. The potent H₁-antagonist astemizole partially inhibited bronchoconstriction without affecting histamine release. Antigen provocation produced a significant increase in circulating levels of the 13,14-dihydro-15-keto metabolite of PGF_2α which could originate from mast cell-derived PGD₂. In both retrospective and prospective studies, a close relationship was shown between nonspecific bronchial reactivity and resting airway calibre in asthma. These data suggest that release of inflammatory mediators are involved in the pathogenesis of the immediate airway response with antigen challenge, and that drugs used to treat asthma may have useful effects, both on the airways and on mediator-secreting cells. Since acquired bronchial hyperreactivity is related to airway inflammation and airway calibre, we propose that pharmacological control of mediator release in vivo represent...

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confidence: 52%

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confidence: 99%

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

Holgate

Benyon

Howarth

et al. 1985

Int Arch Allergy Immunol

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“…Our work extended to an integration of PC metabolic pathway and calcium homeostasis. The elevation of intracellular calcium leads to alteration of phospholipids, especially PC (Moore et al 1984), and also the silencing of PEMT, accelerated the SERCA activity and reduced the ER stress (Jacobs et al 2010). In yeast, the Biological General Repository for Interaction Datasets (BioGRIDs) showed a negative genetic interaction of OPI3 with SPF1 and PMR1 by high throughput screenings (Fig.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress and calcium imbalance are involved in cadmium-induced lipid aberrancy in Saccharomyces cerevisiae

Rajakumar

Bhanupriya

Ravi

2016

Cell Stress and Chaperones

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The endoplasmic reticulum is the key organelle which controls protein folding, lipid biogenesis, and calcium (Ca 2+ ) homeostasis. Cd exposure in Saccharomyces cerevisiae activated the unfolded protein response and was confirmed by the increased Kar2p expression. Cd exposure in wild-type (WT) cells increased PC levels and the PC biosynthetic genes. Deletion of the two phospholipid methyltransferases CHO2 and OPI3 modulated PC, TAG levels and the lipid droplets with cadmium exposure. Interestingly, we noticed an increase in the calcium levels upon Cd exposure in the mutant cells. This study concluded that Cd interrupted calcium homeostasis-induced lipid dysregulation leading to ER stress.

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“…A pivotal role for methionine in modulating the inhibitory effect of stimuli of the oxidative burst on lipid methylation was suggested by the dependency of the effect on the concentration of methyl-donor. Since the intracellular and extracellular pools are readily equilibrated (29), increasing the concentration of methionine in the medium would result in a limitation of the inhibitory effect, possibly by supplying additional amounts of substrate. In a physiologic context, the human plasma concentration of methionine, under usual conditions, may vary from 10 to 40 uM, with fluctuation related to dietary intake (30).…”

Section: Resultsmentioning

confidence: 99%

Activation of the oxidative burst in human monocytes is associated with inhibition of methionine-dependent methylation of neutral lipids and phospholipids.

Bonvini¹,

Bougnoux²,

Stevenson³

et al. 1984

J. Clin. Invest.

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Abstract. Chemotaxis and generation of the oxidative burst by phagocytes are among the biological functions thought to require methylation reaction(s) for their expression. The present study investigated the effect of different stimuli of the oxidative burst on lipid methylation by human elutriated monocytes as measured by methyl group incorporation from [methyl-3H]methionine into both phospholipid and neutral lipid extracts. Normal monocytes, incubated at 370C for 1 h with 2 uM methionine, incorporated 10.2-fmol/106 cells and 73.6-fmol/ 106 cells of methyl groups into neutral lipids and phospholipids, respectively. Stimulators of the respiratory burst, such as the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine, the tumor promoter, 12-0-tetradecanoyl phorbol-13-acetate, and the calcium ionophore, A23 187, decreased the incorporation of methyl groups into both neutral lipids and phospholipids in a similar manner. Increasing the concentration of methionine in the medium reversed or attenuated the inhibition achieved at lower levels. An inverse relationship existed between the degree of methylation and the extent of stimulation of the oxidative burst, measured as superoxide anion (O°) release. Stimulated monocytes oxidized methionine to methionine sulfoxide (which cannot act as a methyl-donor), and this was dependent on activation of the respiratory burst. Elimination of the ac- cumulated methionine sulfoxide by replacement of the medium or by prevention of extracellular methionine oxidation by catalase did not effectively restore the normal level of methylation in stimulated cells, and the reduced methylation was not primarily related to a defective methionine uptake by stimulated monocytes. These data suggest that intracellular events related to activation of the respiratory burst are responsible for the decreased lipid methylation in stimulated cells, possibly by their leading to intracellular formation of methionine sulfoxide and by their limiting the availability of methyl-donor. This mechanism may be of potential relevance for the expression of biological functions where methionine-dependent reactions are involved.

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Calcium signals and phospholipid methylation in eukaryotic cells

Cited by 42 publications

References 59 publications

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

Endoplasmic reticulum stress and calcium imbalance are involved in cadmium-induced lipid aberrancy in Saccharomyces cerevisiae

Activation of the oxidative burst in human monocytes is associated with inhibition of methionine-dependent methylation of neutral lipids and phospholipids.

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