The capacity of basic peptides to trigger exocytosis from mast cells correlates with their capacity to immobilize band 3 proteins in erythrocyte membranes

Dufton, Mark J.; Cherry, Richard J.; Coleman, John W.; Stanworth, D.R.

doi:10.1042/bj2230067

Cited by 29 publications

(3 citation statements)

References 22 publications

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“…Low et al (22) showed an increase in the amount of membrane-bound IgG in normal erythrocytes treated with reagents that promote band 3 aggregation; independently, Dufton et al (23,24) showed that basic peptides can induce aggregation of band 3 molecules. Since knobby parasites synthesize a 90-kDa histidinerich protein, absent from knobless strains (25), it is possible that in the knobby line, the presence of a highly charged protein in the region underlying the erythrocyte plasma membrane (26) produces the increased binding of IgG.…”

Section: Discussionmentioning

confidence: 99%

Expression of senescent antigen on erythrocytes infected with a knobby variant of the human malaria parasite Plasmodium falciparum.

Winograd¹,

Greenan²,

Sherman³

1987

Proc. Natl. Acad. Sci. U.S.A.

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Erythrocytes infected with a knobby variant of Plasmodium falciparum selectively bind IgG autoantibodies in normal human serum. Quantification of membrane-bound IgG, by use of '251-labeled protein A, revealed that erythrocytes infected with the knobby variant bound 30 times more protein A than did noninfected erythrocytes; infection with a knobless variant resulted in less than a 2-fold difference compared with noninfected erythrocytes. IgG binding to knobby erythrocytes appeared to be related to parasite development, since binding of 1251-labeled protein A to cells bearing young trophozoites (less than 20 hr after parasite invasion) was similar to binding to uninfected erythrocytes. By immunoelectron microscopy, the membrane-bound IgG on erythrocytes infected with the knobby variant was found to be preferentially associated with the protuberances (knobs) of the plasma membrane. The removal of aged or senescent erythrocytes from the peripheral circulation is reported to involve the binding of specific antibodies to an antigen (senescent antigen) related to the major erythrocyte membrane protein band 3. Since affinity-purified autoantibodies against band 3 specifically bound to the plasma membrane of erythrocytes infected with the knobby variant of P. fakiparum, it is clear that the malaria parasite induces expression of senescent antigen.Erythrocytes infected with the human malaria parasite Plasmodium falciparum become immunologically altered as a result ofparasite development. These changes, which occur primarily toward the end of the parasite's 48-hr developmental cycle, have been identified by techniques capable of detecting membrane-bound immunoglobulins (1-3). It has been proposed (4) that the newly exposed antigens on the surface of infected erythrocytes are the result of parasitesynthesized proteins that are inserted into the host cell membrane; however, in spite of intense efforts by several laboratories such parasite proteins have been neither fully characterized nor specifically localized, and the manner of transport from the parasite to the erythrocyte surface is yet to be convincingly demonstrated.It is entirely possible that some of the antigenic changes observed for malaria-infected erythrocytes result from parasiteprovoked exposure or modification of host cell antigens. For example, Kay (5) showed that immunoglobulins were specifically bound to the surface of old erythrocytes, and as a result in vitro phagocytosis by macrophages occurred. These autoantibodies, found in the sera ofnormal individuals, bound to the major erythrocyte integral membrane protein, band 3 (6, 7 Elution of membrane-bound IgG was performed according to the procedure of Rekvig and Hannesta (13), except that the incubation time in isotonic glycine buffer was increased to 5 min at 0WC. Cells were layered over a 10% (wt/vol) dextran cushion and centrifuged for 2 min in a Beckman Microfuge. The pelleted cells were washed five to seven times in PBS and then incubated with antibody (70 ,ug/ml) purified by band 3-Sepharose ...

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Section: Discussionmentioning

confidence: 99%

Expression of senescent antigen on erythrocytes infected with a knobby variant of the human malaria parasite Plasmodium falciparum.

Winograd¹,

Greenan²,

Sherman³

1987

Proc. Natl. Acad. Sci. U.S.A.

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“…Stimulation with basic secretagogues, such as anaphylatoxins, neuropeptides, compound 48/80, and poly-L-lysine, results in a distinct Fc3RI-independent pathway for the activation of mast cells (20,21). These stimuli share a common characteristic of being polycations (22)(23)(24), which are able to internalize into or possibly penetrate halfway through the plasma membrane and stimulate the guanine nucleotide-binding proteins (G-proteins) (25,26), ultimately leading to degranulation. A previous structural study of the RBL-2H3 cells activated by this pathway indicates an intermediate surface morphology between the resting cells and antigenactivated cells (11).…”

Section: Introductionmentioning

confidence: 99%

Impact of Actin Rearrangement and Degranulation on the Membrane Structure of Primary Mast Cells: A Combined Atomic Force and Laser Scanning Confocal Microscopy Investigation

Deng

Zink

Chen

et al. 2009

Biophysical Journal

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Degranulation of bone marrow-derived mast cells (BMMCs) triggered by antigens (e.g., 2,4-dinitrophenylated bovine serum albumin (DNP-BSA) and secretagogues (e.g., poly-L-lysine) was investigated by combined atomic force microscopy (AFM) and laser scanning confocal microscopy (LSCM). This combination enables the simultaneous visualization and correlation of membrane morphology with cytoskeletal actin arrangement and intracellular granules. Two degranulation mechanisms and detailed membrane structures that directly corresponded to the two stimuli were revealed. In DNP-BSA triggered activation, characteristic membrane ridges formed in accordance with the rearrangement of underlying F-actin networks. Individual granules were visualized after they released their contents, indicating a "kiss-and-run" pathway. In BMMCs stimulated by poly-L-lysine, lamellopodia and filopodia were observed in association with the F-actin assemblies at and near the cell periphery, whereas craters were observed on the central membrane lacking F-actin. These craters represent a new membrane feature resulting from the "kiss-and-merge" granule fusion. This work provides what we believe is important new insight into the local membrane structures in correlation with the cytoskeleton arrangement and detailed degranulation processes.

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“…S. aureus c~-toxin was isolated (McNiven, Owen & Arbuthnott, 1972) (Dufton et al, 1984) was donated by Dr. R.C. Hider, University of Essex.…”

Section: Pore-forming Agents and Other Chemicalsmentioning

confidence: 99%

Ion modulation of membrane permeability: Effect of cations on intact cells and on cells and phospholipid bilayers treated with pore-forming agents

et al. 1988

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Leakage of ions (Na+, K+) and phosphorylated metabolites (phosphorylcholine, 2-deoxyglucose 6-phosphate) through membrane lesions in intact cells or in cells modified by 'pore-forming' agent has been studied. Leakage from intact cells is induced by protons and by divalent cations such as Cu2+, Cd2+ or Zn2+. Leakage from agent-modified cells--or across phospholipid bilayers modified by agent--is prevented by low concentrations of the same cations and by higher concentrations of Ca2+, Mn2+ or Ba2+; Mg2+, dimethonium, spermine, or spermidine are virtually ineffective. The relative efficacy of a particular cation (e.g. Ca2+) depends more on cell type than on the nature of the pore-forming agent. The predominant effect is on binding of cation to specific sites, not on surface charge. Surface charge, on the other hand, does affect leakage from agent-modified cells in that suspension in nonionic media reduces leakage, which can be restored by increasing the ionic strength: univalent (Na+, K+, Rb+, NH4+) and divalent (Mg2+, dimethonium) cations are equally effective; addition of protons or divalent cations such as Zn2+ to this system inhibits leakage. From this and other evidence here presented it is concluded that leakage across membranes is modulated by the presence of endogenous anionic components: when these are in the ionized state, leakage is favored; when unionized (as a result of protonation) or chelated (by binding to divalent cation), leakage is prevented. It is suggested that such groups are exposed at the extracellular face of the plasma membrane.

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The capacity of basic peptides to trigger exocytosis from mast cells correlates with their capacity to immobilize band 3 proteins in erythrocyte membranes

Cited by 29 publications

References 22 publications

Expression of senescent antigen on erythrocytes infected with a knobby variant of the human malaria parasite Plasmodium falciparum.

Expression of senescent antigen on erythrocytes infected with a knobby variant of the human malaria parasite Plasmodium falciparum.

Impact of Actin Rearrangement and Degranulation on the Membrane Structure of Primary Mast Cells: A Combined Atomic Force and Laser Scanning Confocal Microscopy Investigation

Ion modulation of membrane permeability: Effect of cations on intact cells and on cells and phospholipid bilayers treated with pore-forming agents

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