Disease relevance of Blood Platelets

• Furthermore, a significantly lower than normal serotonin accumulation rate was also detected in dense granules isolated from blood platelets of Down's syndrome individuals [1].
• Augmentation of blood platelet levels by intratracheal administration of an adenovirus vector encoding human thrombopoietin cDNA [2].
• We have examined human and rabbit blood platelets for expression of pp60c-src, the normal cellular homolog of the transforming protein of Rous sarcoma virus. pp60c-src kinase activity was determined by an immune-complex kinase assay that uses enolase as the substrate, and pp60c-src protein levels were determined by an immunoblot assay [3].
• In contrast to the Fab fragments from the autoimmune thrombocytopenia patient who developed SLE, none of the IVIG-selected Fabs from the SLE patient without thrombocytopenia bound to thrombocytes [4].
• In pathophysiologic terms, the reaction of IgG antiglobulin complexes with thrombocytes in vivo may be an important step in the chain of events leading to generalized vascular damage and deposition of immune complexes in vessel walls which is thought to be responsible for the development of generalized vasculitis in RA [5].

Psychiatry related information on Blood Platelets

• We studied acetaminophen sulfation, plasma sulfate levels, and the activity of sulfotransferase in blood platelets in patients with Parkinson's disease, Huntington's disease, and in controls and did not find any abnormality in the patient groups, independent of the use of medication [6].
• Serotonin uptake and imipramine binding in the blood platelets of obsessive-compulsive disorder patients [7].
• We determined serotonin (5-HT) uptake in the blood platelets of Alzheimer's disease (AD) patients and comparable age-matched normal controls [8].
• Altered 5-HT-induced calcium response in the presence of staurosporine in blood platelets from bipolar disorder patients [9].
• Serotonin 5-HT2 receptor binding on blood platelets as a state dependent marker in major affective disorder [10].

High impact information on Blood Platelets

• Upon treatment with agents such as thrombin, collagen or concanavalin A, blood platelets change shape, secrete serotonin and phosphorylate two proteins having molecular weights of approximately 20,000 and 40,000 [11].
• Furthermore, such alpha-actinin/lipid complexes can also be formed in situ during the stimulation of blood platelet aggregation [12].
• Human blood platelets showing no response to collagen fail to express surface glycoprotein Ia [13].
• Blood platelets do not provide endoperoxides for vascular prostacyclin production [14].
• Selective inhibition of thromboxane A2 biosynthesis in blood platelets [15].

Chemical compound and disease context of Blood Platelets

• Endotoxin lipopolysaccharide (LPS) from Acinetobacter 199A induced aggregation of blood platelets from immune adherence-positive species (rat, rabbit) but not from immune adherence-negative species such as pig and man [16].
• Stearic acid causes hypercoagulability of the blood by activation of factor XII and by aggregation of blood platelets [17].
• The incidence of medullary hyperemia was not influenced by inhibiting thrombocyte aggregation with 5 or 70 mg/kg of acetyl salicylic acid or preventing fibrin deposition with 100 IE/kg of heparin before ischemia, and these substances produced no improvement renal function [18].
• Markers of severity of pre-eclampsia, which normalized by 6 months postpartum, included plasma creatinine, uric acid, albumin, endothelin 1 and urinary protein, 2,3, dinor-6-keto-PGF1alpha, blood platelet and neutrophil counts [19].
• No differences were demonstrated between groups for age, preoperative cardiac diagnosis, diabetes, azathioprine, steroid or angiotensin-converting enzyme inhibitor medication, leukocyte and thrombocyte levels, rejection index, or cytomegalovirus (CMV) infection or serostatus [20].

Biological context of Blood Platelets

• Lowering pH in blood platelets dissociates myosin phosphorylation from shape change and myosin association with the cytoskeleton [21].
• In membranes purified from human blood platelets, basal guanosine triphosphate (GTP) hydrolysis is reduced by a factor of approximately 6 by exposure to N-ethylmaleimide (10 mM) [22].
• We report a method designed to distinguish mRNA expression from the two vWF alleles by PCR analysis of peripheral blood platelet RNA using DNA sequence polymorphisms located within exons of the vWF gene [23].
• In summary, a natural dimorphism has been identified within the proximal 5' regulatory region of the human integrin alpha2 gene that is responsible for decreased expression levels of the integrin alpha2beta1 on blood platelets through a mechanism that is probably mediated by the nuclear regulatory proteins Sp1 and Sp3 [24].
• No correlations between TPO mRNA expression and serum TPO concentration, blood platelet count, or gestational age were observed [25].

Anatomical context of Blood Platelets

• In RA, detection of those antibodies was significantly associated with disease activity indices such as serum C-reactive protein (CRP) levels, erythrocyte sedimentation rate, blood platelet counts, and serum IL-6 concentration [26].
• The effects of interferon (IFN) on the arachidonate metabolism and physiological functions of cultured endothelial cells and blood platelets have been examined [27].
• Possible involvement of blood platelet/megakaryocyte system in alpha-1-antitrypsin deficiency [28].
• Comparison of the properties of blood platelets and serotonergic synaptosomes suggests that the human platelet can serve as an appropriate model for the transport, metabolism, and release of serotonin (5-HT) by CNS serotonergic neurons [29].
• However, the coincubation of blood platelets with the leukocytes always resulted in an activation of the C-5 lipoxygenase and formation of (5S)-5-hydroxy-6,8,11,14-icosatetraenoic acid, (5S,12S)-5,12-dihydroxy-6,8,10,14-icosatetraenoic acid, and leukotriene B4 from exogenous arachidonic acid [30].

Associations of Blood Platelets with chemical compounds

• Cytochalasin B, the blood platelet release reaction and cyclic GMP [31].
• Aggregation of human blood platelets induced by adenosine diphosphate or 1-epinephrine was inhibited when the platelets were suspended in plasma which had been previously exposed to an insolubilized omega-aminohexylagarose derivative of prostaglandin E1 [32].
• 2,3-Diphosphoglycerate (2,3-DPG) may inhibit the platelet release reaction and the irreversible aggregation of human blood platelets induced by adenosine diphosphate, epinephrine, or norepinephrine [33].
• 2-Methylthioadenosine[beta-32P]diphosphate. An agonist and radioligand for the receptor that inhibits the accumulation of cyclic AMP in intact blood platelets [34].
• Transfer of adenine nucleotides between the releasable and nonreleasable compartments of rabbit blood platelets [35].

Gene context of Blood Platelets

• Specific complex formation between thrombospondin and histidine-rich glycoprotein may play a significant role in influencing platelet blood vessel wall interactions as well as modulating the association of various cells with the extracellular matrix [36].
• In conclusion, our results demonstrate the expression of the trimolecular complex components (MT1-MMP/TIMP2/MMP2) by blood platelets as well as the ability of MMP inhibitors to modulate the aggregating response [37].
• CD36 associates with CD9 and integrins on human blood platelets [38].
• Coexpression of RAFTK and FAK proteins in megakaryocytic cells and blood platelets was observed [39].
• CXCR4 protein was also detected on peripheral blood platelets [40].

Analytical, diagnostic and therapeutic context of Blood Platelets

• Immunocytochemical localization of fibrinogen, platelet factor 4, and beta thromboglobulin in thin frozen sections of human blood platelets [41].
• METHODS AND RESULTS: Femoral blood flow velocity and ex vivo whole blood platelet aggregation by impedance aggregometry were measured in femoral venous blood during femoral arterial infusion of acetylcholine (ACh; 30 microg/min) in 30 patients, 19 of whom had angiographic atherosclerosis [42].
• By indirect immunofluorescence, we now show that a polyclonal rabbit antibody specific for human glycoproteins IIb plus IIIa and the well-characterized murine monoclonal anti-IIb-IIIa complex antibody, AP2, both crossreact with IIb and IIIa analogs on intact chicken thrombocytes [43].
• By transmission electron microscopy, platelets from the first wave were relatively rounder with a limited number of granules, but platelets from the second wave were discoid shaped with well-developed granules that were indistinguishable from peripheral blood platelets [44].
• Using this compound as an immobilized ligand for affinity chromatography and [3H]S-145 as a radioligand, we have purified the thromboxane A2/prostaglandin H2 receptor from the membranes of human blood platelets [45].

References