ISSN:0953-7104    

DOI:10.3109/09537109209013180

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Platelet activation induced by monoclonal antibodies (mAB) was studied using three stimulatory mAB (all IgG1) against different platelet surface glycoproteins: VM58 against GPIV, LeoAl against PTA1, and FMC 56 against CD9. F(ab')2fragments of these antibodies failed to activate platelets themselves but blocked platelet aggregation induced by the relevant intact antibody. Platelet aggregation was also completely blocked by the anti-FcγRII (Fc-receptor) monoclonal antibody, IV.3. A heterogeneity of platelet response to stimulatory mAB was observed amongst normal donors. All three antibodies added to platelet-rich plasma (PRP) from responders induced full platelet aggregation and dense body release. However, in PRP from nonresponders, VM58 and LeoAl did not induce platelet activation whilst FMC 56 activated platelets but to a lesser extent than in responders (longer lag phase and reduced release). The ratio of responders to nonresponders was∼1:1 (n = 110). The heterogeneity was not due to differences in the copy number of either the antigen (VM58) or FcγRII. The ability of donor platelets to be aggregated by stimulatory mAB in PRP correlated with the ability of these platelets to respond to aggregated murine IgG1(mAB irrelevant to platelets). The combined results suggest that both the Fab and Fc region of stimulatory mAB are necessary in order to induce a platelet response and that this response is mediated through FcγRII. The difference between responders and nonresponders can be explained by the known polymorphism of FcγRII (Looney et al, 1988) and the capacity of the polymorphic forms of FcγRII to bind and to respond to murine IgG1.

ISSN:0953-7104    

DOI:10.3109/09537109209013181

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Previous studies have suggested that platelet Clq receptors share a variety of structural and functional similarities with Clq receptors isolated from Raji cells. The present study extends these observations and demonstrates similar migration of platelet and Raji cell receptors in 7.5% SDS-polyacrylamide gels, as well as similarities in amino acid composition and receptor migration on cellulose acetate electrophoresis at pH 8.6. Moreover, direct functional comparisons were performed to assess receptor reactivity with immobilized Clq and collagen, as structural similarities between collagen and the amino terminus of Clq involved in receptor binding are well known, and Clq inhibits collagen-induced platelet aggregation. Like the platelet Clq receptor, Clq receptors from Raji cells demonstrated enhanced reactivity with Clq relative to collagen-coated surfaces. These interactions were highly susceptible to manipulation of the ionic strength of the buffer medium. Clq receptor recognition of collagen was considerably more sensitive to increasing NaCl concentrations than were receptor interactions with Clq. Platelet and Raji cell Clq receptor adhesion to Clq-coated surfaces occurred at physiologic ionic strength, whereas receptor interactions with collagen were completely inhibited in the presence of greater than 60 mM NaCl. These data suggest that both purified platelet and Raji cell Clq receptors exhibit increased avidity for immobilized Clq as compared to collagen. The biochemical and functional similarities between these receptors support the concept that Clq receptors on platelets and Raji cells may be related.

ISSN:0953-7104    

DOI:10.3109/09537109209013182

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

To investigate in vivo platelet function in acute falciparum malaria plasma concentrations ofβ-thromboglobulin (β-TG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet counts of the 10 patients were significantly lower (p<0.025) than those of the controls, and a slight but significant increase (p<0.05) inβ-TG/PF4 ratios in the patients suggested low-grade platelet activation. Presentation plasmaβ-TG and PF4 concentrations did not differ from control values, probably due to the opposing effects of decreased circulating platelet mass and increased activation. By contrast, admission concentrations of TSP in the surviving patients were markedly lower (p<0.001) than those of the controls;β-TG/PF4 ratios, but not TSP levels, returned to normal during treatment. Hepatic dysfunction and oliguric renal failure probably contributed to a sustained increase in plasmaβ- TG and TSP in the 2 fatally ill patients, but associated elevated PF4 levels indicated concomitant platelet activation. Our results support the suggestion that in vivo platelet activation, which appears to be rapidly controlled by treatment, occurs in patients with severe, non-fatal falciparum malaria. TSP production, apparently from non-platelet sources, was decreased and/or its consumption was increased in these patients, perhaps by factors such as cytoadherence of infected erythrocytes and consequent endothelial damage.

ISSN:0953-7104    

DOI:10.3109/09537109209013183

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Phosphoinositide metabolism in rabbit platelets prelabelled with [32P]phosphate and [3H]inositol was stimulated by platelet activating factor (PAF, 1-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) with stirring at 200 rpm for 120 s in the presence of polymerising fibrin produced by the action of batroxobin (B. atrox) (also referred to by the proprietary name Reptilase) on fibrinogen. Under these conditions platelet-fibrin clots formed and retracted around the stirring bar. Phosphoinositides were extracted with chloroform: methanol: HC1. The role of the secretion of platelet granule contents in the phosphoinositide changes was examined by comparison of the effects of 1 nM PAF which did not cause secretion, with 50 nM PAF which caused extensive secretion. Stimulation of platelets with PAF in the presence of polymerising fibrin caused a greater decrease in the amount and labelling of extractable phosphatidylinositol 4,5-bisphosphate (PIP2) than was observed with platelets stimulated in the presence of fibrinogen. With 1 nM PAF, the decrease (1.26±0.11 nmol/109platelets) in amount of extractable PIP2when platelets were stimulated in the presence of polymerising fibrin compared with in the presence of fibrinogen was accounted for by an increase in the amount of phosphatidylinositol 4-phosphate (PIP). With 50 nM PAF, the decrease in amount of extractable PIP2(1.09±0.11 nmol/109platelets) was not accounted for by an increase in the amount of PIP; the decrease in the amount of [3H]inositol label in PIP2in platelets stimulated in the presence of polymerising fibrin was accounted for by the sum of the increases in PIP labelling and the label associated with interfacial protein from the lipid extractions. When fibrin polymerisation was blocked with glycyl-L-prolyl-L-arginyl-L-proline (GPRP), the large decrease in extractable PIP2and the increase in the association of label with the interfacial protein did not occur. Thus, both the formation of a fibrin network, and the changes that accompany the secretion of granule contents, are necessary for the association of the3H-labelled material with interfacial protein. Blocking thromboxane A2formation had no effect on the changes in response to 50 nM PAF. Although PAF stimulated phospholipase C, resulting in increases in amount and32P-labelling of phosphatidic acid and3H-labelling of inositol bisphosphate and inositol phosphate, the increases were similar in the presence of polymerising fibrin or fibrinogen. Thus, further stimulation of phospholipase C does not occur in association with clot formation. The specific radioactivities of labelling with [3H]inositol of the phosphoinositides in unstimulated platelets differed (PIP2>phosphatidylinositol (PI)>PIP). Upon stimulation of the platelets with 1 nM PAF, the specific radioactivity of PIP rose above that of PI and toward that of PIP2, indicating that the increase in PIP was due to degradation of PIP2. Thus, the large decrease in extractable PIP2and increase in formation of PIP caused by the presence of polymerising fibrin appear to be due to increased degradation of PIP2to PIP.

ISSN:0953-7104    

DOI:10.3109/09537109209013184

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Stripping of cytoplasm from circulating megakaryocytes (MKs) in the pulmonary capillary bed implicates the lungs as an important site for platelet production in normal physiology. The placenta has been proposed as an alternative location for intrauterine platelet production as fetal lungs are essentially non-functioning. To investigate this further, circulating MKs from an umbilical artery and umbilical vein of 10 human placentae were isolated using a modified whole blood filtration technique. Pretreatment of blood, which may be deleterious to MKs, was not required. Following May Grunwald Giemsa staining of filters, MKs were identified by their morphology and classified into 4 types based on subjective assessment of the amount of cytoplasm present. Blood from umbilical arteries and veins contained a mean of 37.2 MKs/0.5 ml (median 37.0; range 17-80) and 23.9 MKs/0.5 ml (median 18.5; range 5-67) respectively (p<0.01). 43% of arterial MKs and 14% of venous MKs possessed copious cytoplasm (p<0.01). These results demonstrate a significant reduction of MK numbers across the placenta. Removal of MK cytoplasm at this site is consistent with the hypothesis that the placenta functions as a platelet forming organ during intrauterine life, the lungs taking over this role after birth.

ISSN:0953-7104    

DOI:10.3109/09537109209013185

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109209013186

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

The Endothelium. An Introduction to Current Research Edited by John B Warren, Wiley-Liss Inc., New York 1990. 317 pages. Price $54.95 (hardback)

ISSN:0953-7104    

DOI:10.3109/09537109209013187

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109209013188

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor