Platelet Shape Change

2017 ◽  
pp. 321-336 ◽  
Author(s):  
Joseph E. Aslan
Keyword(s):  
Shape Change ◽  
Platelet Shape

Platelet Aggregation Caused by Dithiothreitol

1984 ◽  
Vol 51 (01) ◽  
pp. 119-124 ◽  
Author(s):  
M B Zucker ◽  
N C Masiello
Keyword(s):  
Shape Change ◽  
Blood Platelets ◽  
Dense Granule ◽  
Metabolic Inhibitors ◽  
Electrophoretic Patterns ◽  
Discernible Effect ◽  
Variable Extent ◽  
Triton X ◽  
Induced Aggregation ◽  
Platelet Shape

SummaryMacIntyre et al. showed that over 1 mM dithiothreitol (DTT) aggregates blood platelets in the presence of fibrinogen; aggregation is not inhibited by prostaglandin E1. We confirmed their data and found that 70 mM 2-mercaptoethanol was also active. DTT- induced aggregation was not associated with platelet shape change or secretion of dense granule contents, was not inhibited by tetracaine or metabolic inhibitors, was prevented at pH 6.5, and prevented, reversed, or arrested by EDTA, depending on when the EDTA was added. DTT did not cause aggregation of thrombasthenic, EDTA-treated, or cold (0° C) platelets, which also failed to aggregate with ADP. Platelets stimulated with DTT bound 125I-labeled fibrinogen. Thus DTT appears to “expose” the fibrinogen receptors. SDS gel electrophoresis of platelet fractions prepared by use of Triton X-114 showed that aggregating concentrations of DTT reduced proteins of apparent Mr 69,000 and 52,000 (probably platelet albumin) and, to a variable extent, glycoproteins Ib, IIb and III. Exposure of unlabeled or 125I- labeled platelets to ADP had no discernible effect on the electrophoretic patterns.

Adenosine Diphosphate (ADP)-Induced ⍺-Granules Release from Platelets of Native Whole Blood Is Reduced by Ticlopidine but Not by Aspirin or Dipyridamole

1986 ◽  
Vol 56 (02) ◽  
pp. 147-150 ◽  
Author(s):  
V Pengo ◽  
M Boschello ◽  
A Marzari ◽  
M Baca ◽  
L Schivazappa ◽  
...  
Keyword(s):  
Whole Blood ◽  
Light Transmission ◽  
Ex Vivo ◽  
Early Stage ◽  
Shape Change ◽  
Adenosine Diphosphate ◽  
Dose Dependent ◽  
Plateletderived Growth Factor ◽  
Platelet Shape

SummaryA brief contact between native whole blood and ADP promotes a dose-dependent release of platelet a-granules without a fall in the platelet number. We assessed the “ex vivo” effect of three widely used antiplatelet drugs, aspirin dipyridamole and ticlopidine, on this system. Aspirin (a single 800 mg dose) and dipyridamole (300 mg/die for four days) had no effect, while ticlopidine (500 mg/die for four days) significantly reduced the a-granules release for an ADP stimulation of 0.4 (p <0.02), 1.2 (p <0.01) and 2 pM (p <0.01). No drug, however, completeley inhibits this early stage of platelet activation. The platelet release of α-granules may be related to platelet shape change of the light transmission aggregometer and may be important “in vivo” by enhancing platelet adhesiveness and by liberating the plateletderived growth factor.

scholarly journals Evidence for a role of myosin phosphorylation in the initiation of the platelet shape change response.

1984 ◽  
Vol 259 (15) ◽  
pp. 9826-9831
Author(s):  
J L Daniel ◽  
I R Molish ◽  
M Rigmaiden ◽  
G Stewart
Keyword(s):  
Shape Change ◽  
Myosin Phosphorylation ◽  
Change Response ◽  
Platelet Shape

scholarly journals Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 2016-2021 ◽  
Author(s):  
RI Parker ◽  
HR Gralnick
Keyword(s):  
Von Willebrand Factor ◽  
Shape Change ◽  
Adenosine Diphosphate ◽  
Surface Expression ◽  
Platelet Surface ◽  
Granule Secretion ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Platelet Shape ◽  
Stimulation Of

Abstract Platelets contain a pool of endogenous platelet-von Willebrand factor (vWF) that becomes expressed on the platelet surface when platelets are stimulated by a variety of agonists. Maximal platelet-vWF expression occurs in concert with platelet alpha-granule secretion. Aspirin (ASA) is known to impair platelet activation and alpha-granule secretion by irreversible inhibition of platelet cyclo-oxygenase. We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin. We found that each agonist was effective in promoting increased platelet- vWF surface expression on native and ASA-treated platelets. ASA-treated platelets responded identically to native platelets to low (0.01 U/mL) and high (1.0 U/mL) concentrations of thrombin, while the ADP-induced increase in ASA-treated platelets was only 50% to 60% of that for control platelets. Measurement of secreted platelet-vWF and beta- thromboglobulin indicated that the increase seen with ADP was largely independent of alpha-granule secretion. Using monoclonal antibodies (MoAbs) against the platelet glycoproteins (GP) IIb/IIIa and Ib (MoAbs 10E5 and 6D1, respectively), we demonstrated that the ADP-induced increase in platelet-vWF expression on control platelets primarily involved the binding of secreted platelet-vWF to the platelet GPIIb/IIIa. In contrast, the increase in platelet-vWF that occurred following ADP stimulation of ASA-treated platelets was largely insensitive to GPIIb/IIIa blockade. No effect of GPIb blockade in platelet-vWf expression was noted for either control or ASA-treated platelets. When platelet shape change was prevented by the addition of cytochalasin D, ADP-induced platelet-vWf surface expression on ASA- treated platelets was reduced by more than 80%. Our data indicate that platelets in which the cyclooxygenase pathway is blocked by the action of aspirin can increase surface expression of platelet-vWf as a consequence of platelet shape change. We speculate that this process exposes platelet-vWf bound to GPIIb/IIIa, or possibly GPIb, within the surface connected canalicular system.

Changes In Triphosphatidylinositol Metabolism During PGE1- Induced Shape Change Of Washed Rabbit Platelets

1981 ◽  
Author(s):  
J D Vickers ◽  
R L Kinlough-Rathbone ◽  
J F Mustard
Keyword(s):  
Phosphatidic Acid ◽  
Shape Change ◽  
Specific Radioactivity ◽  
Inositol Phospholipids ◽  
Rabbit Platelets ◽  
Turn Over ◽  
Camp Levels ◽  
Camp Formation ◽  
Platelet Shape ◽  
Stimulation Of

Since the inositol phospholipids are present in small amounts in platelets and turn over rapidly during platelet shape change, aggregation and release, they are thought to have a functional rather than structural role in platelets. We have previously reported that within 10 sec of stimulation of prelabeled, washed rabbit platelets with ADP, the amount of triphosphatidylinositol (TPI) is significantly reduced while the specific radioactivity of its [32p]phosphate is increased. One explanation of this result is that ADP- stimulation may divert ATP required for phosphorylation of diphosphatidylinositol (DPI) to TPI, leading to a decrease in the amount of TPI. PGE1 (10 μM) causes conversion of ATP to cAMP and induces a transient platelet shape change. The shape change may be due to the reduction in ATP with a concomitant fall in TPI. We have therefore studied whether PGE1-stimulation of washed rabbit platelets prelabeled with [32P] causes a change in TPI. Within 10 sec the amount of TPI in PGE1-treated platelets was reduced from 2.22 nmoles/ 109 platelets to 1.98 nmoles/109 platelets (p<0.05) although neither the [32P] labeling (51.1 × 103 dpm/109 platelets) nor specific radioactivity (24.1 × 103 dpm/nmole) were significantly changed. These results are compatible with the theory that diversion of ATP by PGE1-stimulation of cAMP formation from ATP, may reduce the amount of TPI. A similar effect was observed previously with ADP-stimulation. PGE1 caused no change in the [32p] labeling of phosphatidic acid (PA) (ADP caused a 290% increase) and caused only a small increase in its specific radioactivity (16% compared to 270% with ADP). If the rates of turnover of TPI and PA which are reflected in their specific radioactivities are Ca2+- dependent, Ca2+ sequestration due to increased cAMP levels induced by PGE1 would, after the initial effects, terminate these changes. The results further support the suggestion that reduction in the amount of TPI may be involved in platelet shape change and initiation of aggregation.

Light Scattering and Platelet Aggregation

1975 ◽  
Author(s):  
J. F. Stoltz ◽  
A. Larcan ◽  
J. F. Batoz ◽  
F. Streif
Keyword(s):  
Experimental Study ◽  
Light Scattering ◽  
Platelet Aggregation ◽  
Shape Change ◽  
Light Variation ◽  
Aggregation Kinetics ◽  
Specific Absorption ◽  
Nephelometric Method ◽  
Platelet Concentration ◽  
Platelet Shape

After a short recall of the theories concerning nephelometry and light scattering, the authors develop their experimental study, which is divided into three parts :- platelets absorption i.e. wave lengths- light variation curves transmitted or scattered according to platelet concentration- aggregation by nephelometric method and by light scattering.These experiments allow the authors to conclude that platelets do not present a specific absorption; that the variations of the light transmitted or scattered is exponential in function of the platelet concentration and that the aggregation test affords essentially a measurement of the decrease of the number of free platelets in the medium.Besides, they observe that the measures of aggregation kinetics, or the problem of platelet shape change are not specific and should be investigated with the help of other methods.This work was supported by D. R. M. E. grant (Biological Section).

ADP-induced inhibition of von Willebrand factor-mediated platelet agglutination

1976 ◽  
Vol 230 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
RA Grant ◽  
MB Zucker ◽  
J McPherson
Keyword(s):  
Human Plasma ◽  
Von Willebrand Factor ◽  
Prostaglandin E1 ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Normal Human ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Formalin Fixed ◽  
Platelet Shape

Human plasma von Willebrand factor (vWF) plus the antibiotic ristocetin, or bovine or porcine vWF alone, agglutinates platelets in either normal human ethylenediaminetetraacetate (EDTA)-treated citrated platelet-rich plasma (PRP) or citrated PRP from patients with the congenital platelet defect thrombasthenia. The prior addition of 1-10 muM ADP, which causes platelet shape change but not aggregation under these conditions, inhibited vWF-mediated agglutination. Inhibition was prevented by 200 muM ATP. Addition of ADP caused prompt reversal of established vWF-mediated agglutination, which resumed when the ADP was enzymatically removed. EDTA-treated, Formalin-fixed, washed normal platelets also underwent vWF-mediated agglutination. ADP was inhibitory only when added before fixation. Epinephrine (40 muM), prostaglandin E1 (7 muM), or serotonin (2 muM) added before fixation caused slight to moderate inhibition but always less than ADP. Platelets from blood chilled before fixation were fully active. Platelets fixed in freshly prepared PRP did not agglutinate as well as those fixed after incubation of PRP, probably because centrifugation exposes the platelets to ADP. It concluded that ADP causes a reversible decrease in the accessibility of the membrane receptor to vWF.

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