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At least 127 records · Page 7Linked to original sources
PubMed1998

Peptide LSARLAF activates alpha(IIb)beta3 on resting platelets and causes resting platelet aggregate formation without platelet shape change.

Adhesion of resting platelets to fibrinogen was enhanced by a peptide which was designed to bind near the presumptive fibrinogen gamma-chain binding site of the alpha subunit of the integrin alpha(IIb)beta3. This peptide, but not a scrambled control peptide, induced adhesion of resting platelets to fibronectin, vitronectin, von Willebrand factor, and monovalent (lacks one functional gamma-chain) fibrinogen. Resting platelets not treated with the agonist peptide did not adhere to these ligands. Agonist peptide induced adhesion of resting platelets to Fg was not secretion dependent and was inhibited by the monoclonal antibody 7E3. The agonist peptide caused aggregation of resting platelets on resting platelets adherent to immobilized Fg without causing platelet shape change. Therefore, the agonist peptide may activate alpha(IIb)beta3 by directly inducing a conformation change in the receptor on resting platelets.

Adenosine Diphosphate↗
PubMed2003

Evidence for a role for Galphai1 in mediating weak agonist-induced platelet aggregation in human platelets: reduced Galphai1 expression and defective Gi signaling in the platelets of a patient with a chronic bleeding disorder.

We have examined platelet functional responses and characterized a novel signaling defect in the platelets of a patient suffering from a chronic bleeding disorder. Platelet aggregation responses stimulated by weak agonists such as adenosine diphosphate (ADP) and adrenaline were severely impaired. In comparison, both aggregation and dense granule secretion were normal following activation with high doses of collagen, thrombin, or phorbol-12 myristate-13 acetate (PMA). ADP, thrombin, or thromboxane A2 (TxA2) signaling through their respective Gq-coupled receptors was normal as assessed by measuring either mobilization of intracellular calcium, diacylglycerol (DAG) generation, or pleckstrin phosphorylation. In comparison, Gi-mediated signaling induced by either thrombin, ADP, or adrenaline, examined by suppression of forskolin-stimulated rise in cyclic AMP (cAMP) was impaired, indicating dysfunctional Galphai signaling. Immunoblot analysis of platelet membranes with specific antiserum against different Galpha subunits indicated normal levels of Galphai2,Galphai3,Galphaz, and Galphaq in patient platelets. However, the Galphai1level was reduced to 25% of that found in normal platelets. Analysis of platelet cDNA and gDNA revealed no abnormality in either the Galphai1 or Galphai2 gene sequences. Our studies implicate the minor expressed Galphai subtype Galphai1 as having an important role in regulating signaling pathways associated with the activation of alphaIIbbeta3 and subsequent platelet aggregation by weak agonists.

Adenosine Diphosphate↗
PubMed1986

Deficiency of platelet membrane glycoprotein Ia associated with a decreased platelet adhesion to subendothelium: a defect in platelet spreading.

A bleeding disorder with absent collagen-induced platelet aggregation and adhesion has been described in a patient whose platelets failed to express surface glycoprotein Ia. We studied the interaction of her platelets with subendothelium in an annular perfusion chamber and the interaction with purified human collagen type III in a rectangular perfusion system under flow conditions. Platelet adherence was almost completely absent both at low and high shear rates. The few platelets which adhered remained in the contact stage without subsequent spreading and aggregate formation. Addition of a monoclonal antibody, which was directed against the von Willebrand moiety of FVIII-VWF, to the blood, completely abolished platelet adherence at high shear rates and had a partial effect at low shear rates. These data indicate that von Willebrand factor plays a role in the initial attachment (contact stage) of platelets to subendothelium. We conclude that the bleeding disorder and excessively prolonged bleeding time in our patient are caused by a new specific defect of the platelet-vessel wall interaction.

Blood Coagulation Disorders↗
PubMed1984

Activation of phospholipase C is dissociated from arachidonate metabolism during platelet shape change induced by thrombin or platelet-activating factor. Epinephrine does not induce phospholipase C activation or platelet shape change.

The present study compares the molecular mechanism by which thrombin, platelet-activating factor, and epinephrine induce platelet activation. Thrombin and platelet-activating factor induce an initial activation of phospholipase C, as measured by formation of 1,2-diacylglycerol and phosphatidic acid, during platelet shape change which is independent of and dissociated from metabolism of arachidonic acid. Phospholipase C activation and shape change are independent of extracellular Ca2+ and Mg2+. Formation of cyclooxygenase products occurs subsequent to the initial activation of phospholipase C and those metabolites are associated with platelet aggregation and further activation of phospholipase C. On the other hand, epinephrine is an unique platelet stimulus since it requires extracellular divalent cations and does not induce platelet shape change or activation of phospholipase C. Our results indicate that activation of phospholipase C may be a mechanism by which physiological agonists can activate platelets independently of extracellular divalent cations.

Arachidonic Acid↗
PubMed2001

Augmented oxidative stress of platelets in chronic smokers. Mechanisms of impaired platelet-derived nitric oxide bioactivity and augmented platelet aggregability.

OBJECTIVES: We investigated whether impaired platelet-derived nitric oxide (PDNO) bioactivity and augmented platelet aggregability in chronic smokers are related to the imbalance of the intraplatelet redox state through increased oxidative stress. BACKGROUND: Chronic smoking impairs PDNO release and augments platelet aggregability. However, their mechanisms are unknown. METHODS: Collagen-induced PDNO release, platelet aggregation, plasma and intraplatelet vitamin C and reduced glutathione (GSH), intraplatelet cyclic guanosine 3',5'-monophosphate (cGMP) and intraplatelet nitrotyrosine production, which is a marker of the peroxynitrite formation, were measured in 11 chronic smokers and 10 age-matched nonsmokers. RESULTS: Release of PDNO and levels of intraplatelet cGMP were lower, and platelet aggregation was greater, in smokers than in nonsmokers. Intraplatelet vitamin C and GSH levels were lower in smokers than in nonsmokers. Intraplatelet nitrotyrosine production was greater in smokers than in nonsmokers. Next, we investigated the effects of oral vitamin C administration (2 g). After vitamin C administration, intraplatelet vitamin C levels were increased and not different at 2 h between the two groups. Then, PDNO release, intraplatelet cGMP levels and platelet aggregation in smokers were restored to the levels of nonsmokers. In smokers, PDNO release and consumption of GSH during platelet aggregation were inversely correlated, and consumption was much less after vitamin C administration. Vitamin C administration decreased intraplatelet nitrotyrosine production in smokers. CONCLUSIONS: Impaired PDNO bioactivity and augmented platelet aggregability may be caused by an imbalance of the intraplatelet redox state through increased oxidative stress in smokers.

Administration, Oral↗
PubMed1997

Cytokines in platelet concentrates: a comparison of apheresis platelet (haemonetics) and filtered and unfiltered pooled buffy-coat derived platelet concentrates.

Variable degrees of platelet activation, shape changes, microvesiculation and fragmentation may occur during collection, processing and storage of platelet concentrates (PCs), contributing to different rate of platelet storage lesion. Leukocytes contribute to both the frequency of transfusion reactions and the acceleration of the rate of platelet storage lesion hence leukocyte removal of platelet concentrates has been introduced to overcome these problems. However transfusion reaction can still occur with the use of leuko-reduced products and it is not fully elucidated that the rate of storage lesion is equivalent for filtered and unfiltered counter parts. This issue has been addressed in this manuscript comparing the generation of cytokines during storage in PCs derived from pooled buffy coat with the standard apheresis products, with a similar level of leukocyte contamination. The EDTA-induced shape change in platelet was used as an index of platelet functional integrity. In addition IL-8 and TGF beta were used as indicators of filtration process-inducing stimulation of cytokines. Our results clearly indicate that a rapid disc/spheric conversion occurs during storage of buffy-coat derived PC, and while prestorage filtration reduces both IL-8 content immediately after filtration and at the end of platelet shelf life but such a process may lead to slight enhancement of the rate of TGF beta generation indicating that any additional process may have some bearing in stimulation of TGF beta release.

Blood Platelets↗
PubMed2004

Role of platelet-derived growth factor in mesangium development and vasculopathies: lessons from platelet-derived growth factor and platelet-derived growth factor receptor mutations in mice.

PURPOSE OF REVIEW: The phenotypic consequences of null mutations in the platelet-derived growth factor-B and the platelet-derived growth factor beta-receptor genes in mice have demonstrated that these proteins play pivotal roles in the development of the vascular smooth muscle cell lineage, including pericytes and mesangial cells. RECENT FINDINGS: The lethality of these mutants has precluded analysis of the physiological and pathophysiological consequences of platelet-derived growth factor-B and platelet-derived growth factor beta-receptor deficiency in adults. This review summarizes and discusses recent data from certain tissue-specific and subtle mutations in the platelet-derived growth factor-B and platelet-derived growth factor beta-receptor genes that are compatible with postnatal viability in spite of severe developmental deficits in pericyte and mesangial cell recruitment. In the postnatal period, the animals studied developed a characteristic set of pathological changes to small blood vessels of the retina and the kidney glomerulus, which sheds light on the importance of pericytes and mesangial cells for vascular integrity and function after birth. SUMMARY: These microvascular abnormalities and their consequences bear a resemblance to diabetic microangiopathy and nephropathy. The platelet-derived growth factor-B and platelet-derived growth factor beta-receptor mutant mouse models, therefore, might serve as valuable tools in the dissection of some of the pathogenic events in diabetic microangiopathy.

Animals↗
PubMed2005

Platelet size deviation width, platelet large cell ratio, and mean platelet volume have sufficient sensitivity and specificity in the diagnosis of immune thrombocytopenia.

We investigated the significance of the platelet indices, mean platelet volume (MPV), platelet size deviation width (PDW), and platelet-large cell ratio (P-LCR), in the diagnosis of thrombocytopenia by comparing these levels in 40 patients with hypo-productive thrombocytopenia (aplastic anaemia; AA) and 39 patients with hyper-destructive thrombocytopenia (immune thrombo-cytopenia; ITP). The sensitivity and specificity of platelet indices to make a diagnosis of ITP were also compared. All platelet indices were significantly higher in ITP than in AA, and platelet indices showed sufficient sensitivity and specificity. The area under the curve (AUC) of the receiver operating characteristics curve of platelet indices was large enough to enable the diagnosis of ITP. P-LCR and PDW had the largest AUCs, which indicated that these values were very reliable for immune thrombocytopenia. Our results suggest that these indices provide clinical information about the underlying conditions of thrombocytopenia. More attention should be paid to these indices in the diagnosis of thrombocytopenia.

Adult↗
PubMed1988

Characterization of human platelet vasopressin receptor and the relation between vasopressin-induced platelet aggregation and vasopressin binding to platelets.

Immunoreactive AVP was found to be much higher in platelets than in platelet-free plasma (PFP) in normal subjects (12.8 +/- 6.3 versus 1.7 +/- 0.8 fmol/ml). AVP levels in PFP were appreciably elevated in parallel with the elevation of plasma osmolality induced by the acute osmotic stimulation, while the AVP levels in platelets did not change before and after the stimulation. Binding studies on intact platelets demonstrated specific binding sites for [3H]AVP. The specific binding was time, temperature and concentration-dependent, saturable and reversible, with the maximal binding capacity (Bmax) of 169.9 +/- 14.4 sites/platelet and affinity of 4.84 +/- 1.15 x 10(8)M-1. The affinity constants for unlabelled AVP, lysine vasopressin (LVP), oxytocin (OT) and dDAVP were 9.0, 8.5, 7.4 and 6.6, respectively, and the inhibition constant for d(CH2)5Tyr(Me)AVP (V1-antagonist) was 7.7. There was a highly significant correlation between the affinity constants of AVP analogues and their relative vasopressor activities in vivo, whereas no such correlation was found between the affinity constants and antidiuretic activities. AVP caused platelet aggregation with the maximal aggregation of 48.0 +/- 25.1% at 230 nM of AVP. A significant correlation was observed between the maximal percentage aggregation and Bmax of [3H]AVP to intact platelets. These results suggest that the platelet vasopressin receptor belongs to the V1 vascular subtype and mediates platelet aggregation.

Adult↗
PubMed1991

Superoxide dismutase cooperates with prostacyclin to inhibit platelet aggregation: a comparative study in washed platelets and platelet rich plasma.

The role of superoxide anions (O2-) in human platelet aggregation in Krebs' buffer or plasma was investigated. In indomethacin (10 microM)-treated washed platelets superoxide dismutase (SOD; 60 U/ml) or ferricytochrome c (FCC; 70 microM) inhibited platelet aggregation by thrombin but not that by collagen or ADP. In addition, in indomethacin (10 microM)-treated washed platelets, SOD significantly potentiated the anti-aggregatory activity of prostacyclin (PGI2) or iloprost when thrombin but not collagen was used as the aggregating agent. In platelet rich plasma, SOD (60 U/ml) did not inhibit platelet aggregation nor did it potentiate the anti-aggregatory activity of iloprost when ADP, collagen or thrombin were used as aggregating agents. Thus, O2- participate in the aggregatory activity of thrombin but not collagen or ADP and PGI2 or iloprost, by reducing the sensitivity of platelets to thrombin, co-operate with SOD to inhibit thrombin-induced platelet aggregation. The interpretation of the use of SOD in experiments involving endothelium-derived relaxing factor (NO) is discussed.

Adenosine Diphosphate↗
PubMed1989

[Relation of the level of platelet membrane glycoproteins, platelet adhesion, platelet aggregation and traditional Chinese medicine syndrome patterns of coronary heart disease].

This experiment made quantitative analysis of platelet GPlb of 56 patients with coronary heart disease and with McAb SZ-2 resisting to human being platelet GP by using the method of indirect immunity fluorescence saturation, observed the changes of coronary heart patients' platelet GPlb based on TCM differentiation of the pattern, and determined the level of PAdT, PAgT. The results showed that the level of platelet GPlb of coronary heart disease was higher than normal. Among them, the acute myocardiac infarction group was the most obvious, followed by the unstable angina pectoris group and the stable angina pectoris group. The level of PAdT, PAgT of coronary heart patients was higher than those of the normal group (P less than 0.005, 0.05); the level of platelet GPlb in blood stasis syndrome group was higher remarkably than the group of having no blood stasis syndrome and the normal (P less than 0.001). These results suggested that it played an important part in the occurrence and development of coronary heart disease as manifested by abnormal increase of platelet GPlb, and enhancement of platelet's adherence and aggregation. The abnormal increase of platelet GPlb is due to pathological mechanism of blood stasis syndrome of coronary heart disease. This experiment also provided a fresh evidence to TCM differentiation of the pattern and treatment of coronary heart disease.

Adult↗
PubMed1988

Platelet parameters. Part I. Platelet counts and mean platelet volume in normal and pregnant subjects.

Platelet counts and mean platelet volume (MPV) were studied in 564 normal subjects and 297 pregnant women using a Coulter Model S-Plus electronic counter. The reproducibility of these measurements both intra- and inter-sample was documented. The mean platelet count in the normal group was 283 x 10(9)/l while the mean MPV was 9.32 fl. An inverse correlation between platelet volume and platelet number was documented (r = -0.38; P less than 0.0001). By interval analysis, this inverse relationship was shown to be non-linear. In the pregnant subjects there appeared to be a progressive decrease in platelet count with advancing gestation; this reached a significant level when the first and third trimesters were compared with each other (P less than 0.05). The MPV was unchanged. The fact that the platelet count decreased in proportion to the red cell count suggested that a common factor, such as haemodilution, was in part responsible. There was again an inverse relationship between MPV and platelet number (r = -0.39; P less than 0.0001) shown to be non-linear by interval analysis.

Blood Platelets↗
PubMed1995

[Shear-induced platelet aggregation (SIPA) monitoring of hemostatic effect during platelet transfusion in a patient with Glanzmann's thrombasthenia: a comparison between SIPA and conventional platelet aggregation].

Shear-induced platelet aggregation (SIPA) in a patient with Glanzmann's thrombasthenia was examined during platelet infusion therapy. Prior to platelet infusion, SIPA measured with the modified cone-and-plate type viscometer, as well as ADP-and collagen-induced platelet aggregation measured with the conventional platelet aggregometer, were absent. The patient's SIPA after multiple infusions of platelet, in parallel with the bleeding time and the clinical hemostatic effect, improved to the normal level, while ADP-and collagen-induced platelet aggregation remained abnormal. These observations imply that SIPA is physiologically more relevant than the conventional agonist-induced platelet aggregometry in this type of the disease.

Adenosine Diphosphate↗
PubMed1989

Sheep platelets as a model for human platelets: evidence for specific PAF (platelet activating factor) receptors.

In a number of animals, the platelet response to Platelet Activating Factor (PAF) has been shown to differ considerably from that in humans. However, aggregation, release and particularly shape change were quite similar for human and sheep platelets. In this study, aggregation and shape change analysis were used to measure the response of sheep platelets to various synthetic analogs of PAF. Response is greatly reduced with no alkyl group in position 2 of PAF and decreases progressively as the number of carbons of the alkyl gets larger than three. A reduction of activity is also seen as the ether linkage at position 1 of PAF is replaced by an ester linkage. These changes are indicative of a specific membrane receptor for PAF in sheep platelets and confirm the usefulness of sheep platelets as a model for PAF-platelet interaction in humans.

Animals↗
PubMed1988

Lipoxygenase activities of human platelets and their subcellular fractions: comparison between lipoxygenase-deficient platelets and normal platelets.

Lipoxygenase activities were estimated in washed platelets (intact platelets) and their subcellular fractions obtained from 7 patients with deficient platelet lipoxygenase activities and 9 normal subjects. From sonicated platelet preparations, 12,000 g supernatant (F-I), cytosol (F-II) and microsomal fractions (F-III) were prepared by differential centrifugation. When 12-hydroxyeicosatetraenoic acid (12-HETE) produced by the incubation of arachidonic acid with intact platelets or each of their subcellular fractions from normal subjects was measured by reversed-phase high-performance liquid chromatography analysis, the lipoxygenase activities of F-I, F-II and F-III were 87%, 31% and 17%, respectively, of the enzyme activity of intact platelets. One of the patients showed no detectable lipoxygenase activity in any preparation, while the other patients showed reduced enzyme activities in all preparations. The addition of CaCl2 significantly increased 12-HETE synthesis solely by F-I from these patients. In most of these patients, contrary to normal subjects, it appeared that the lipoxygenase activity was not fully expressed in intact platelets, since the F-I produced more 12-HETE than the intact platelets.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Refractoriness to platelet transfusion after single-donor consecutive platelet transfusions and its relationship to platelet antibodies.

In thirty patients with acute leukemia and severe aplastic anemia receiving random single donor platelet transfusions, the development of refractoriness by consecutive platelet transfusions with cytapheresis and its relationship to the appearance of anti-platelet antibodies were investigated. The median number of platelet transfusions inducing refractoriness was 13 times, and 20% of the patients remained unrefractory despite of the repeated multiple platelet transfusions up to 20 to 25 times. The results of anti-platelet antibody tasts by the enzyme-linked immunosorbent assay(ELISA) and immunofluorescent techniques(IFT) showed no statistically significant relationship with the refractoriness (p greater than 0.1). Although there was significant correlation between the results of ELISA and IFT, both tests were insufficient to find out refractoriness even with the use of pooled platelets from multiple donors as target cells. This study shows that 13 single donor platelet transfusions result in refractoriness, that both ELISA and IFT are insufficient to detect refractoriness despite of their significant correlation, and that other methods than these are needed in order to detect alloimmunization.

Adolescent↗