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中国输血杂志 2017年第6期30卷 558-562页

作者：杨江存袁军孙杨马婷胡兴斌王文华谢昕昕张小乐顾顺利陈萍尹文陕西省人民医院输血科陕西西安710068 第四军医大学西京医院输血科

目的对比分析4℃冷藏保存血小板与22℃振荡保存血小板代谢情况,为制定冷藏保存血小板技术提供实验室依据。方法对4℃冷藏保存血小板于保存到d1、d3、d5、d7、d10、d14、d21,7个时间点和22℃振荡保存血小板保存到d1、d3、d5,3个时间点时... 详细信息

目的对比分析4℃冷藏保存血小板与22℃振荡保存血小板代谢情况,为制定冷藏保存血小板技术提供实验室依据。方法对4℃冷藏保存血小板于保存到d1、d3、d5、d7、d10、d14、d21,7个时间点和22℃振荡保存血小板保存到d1、d3、d5,3个时间点时采集血样,检测不同保存条件下的血小板血气指标、生物化学指标和低渗休克反应率。结果 4℃冷藏保存血小板在保存7 d内pH、Na^+、Ca^(2+)、Cl^-值无明显变化(P>0.05),22℃振荡保存血小板pH、Na^+、Ca^(2+)、Cl^-、PCO_2、PO_2、Lac、HCO_3^-、ctCO_2、Gap(K^+)保存5 d内均有明显变化(P<0.05)。血小板保存d5时,22℃保存血小板的pH值明显低于4℃保存血小板,而LDH和Lac值明显高于4℃保存(P<0.05)。LDH、pH、K^+、PCO_2、PO_2、Lac、HCO_3^-、ctCO_2、Gap(K^+)2组间比较均有差异(P<0.05)。4℃冷藏保存5 d内血小板低渗休克恢复率变化不明显(P>0.05),而22℃保存血小板HSR恢复率d5与d1相比降低53.77%。结论 4℃冷藏保存血小板与22℃振荡保存血小板在代谢方面比较,冷藏保存血小板具有代谢慢、乳酸产生少、pH降低慢及葡萄糖消耗低等特点,4℃冷藏保存血小板10-14 d时仍有一定的HSR恢复率。就血小板代谢数据比较,4℃冷藏保存血小板建议保存10-14 d。

关键词：冷藏保存血小板/代谢

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Interaction of linker for activation of T cells with multiple adapter proteins in platelets activated by the glycoprotein VI-selective ligand, convulxin

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第43期275卷 33427-33434页

作者： Asazuma, N Wilde, JI Berlanga, O Leduc, M Leo, A Schweighoffer, E Tybulewicz, V Bon, C Liu, SK McGlade, CJ Schraven, B Watson, SP Univ Oxford Dept Pharmacol Oxford OX1 3QT England Heidelberg Univ Inst Immunol D-69120 Heidelberg Germany Inst Pasteur Unite Venens F-75724 Paris 15 France Univ Toronto Hosp Sick Children Res Inst Dept Med Biophys Toronto ON M5G 1X8 Canada Natl Inst Med Res Div Cellular Immunol London NW7 1AA England

The snake venom toxin convulxin activates platelets through the collagen receptor glycoprotein VI (GPVI)/Fc receptor gamma -chain (FcR gamma -chain) complex leading to tyrosine phosphorylation and activation of the tyrosine Syk and phospholipase C gamma2 (PLC gamma2), In the present study, we demonstrate that convulxin is a considerably more powerful agonist than collagen or the GPVI-selective collagen-related peptide (CRP), Confirmation that the response to convulxin is mediated solely via Syk was provided by studies on Syk-deficient platelets. The increase in phosphorylation of the FcR gamma -chain is associated with marked increases in tyrosine phosphorylation of downstream proteins including Syk, linker for activation of T cells (LAT), SLP-76, and PLC gamma2, The transmembrane adapter LAT coprecipitates with SLP-76 and PLC gamma2, as well as with a number of other adapter proteins, some of which have not been previously described in platelets, including Cbl, Grb2, Gads, and SKAP-HOM. Cads is constitutively associated with SLP-76 and is probably the protein bridging its association with LAT, There was no detectable association between Grb2 and SLP-76 in control or stimulated cells, suggesting that the interaction of LAT with Grb2 is present in a separate complex to that of LAT Gads SLP-76. These results show that the trimeric convulxin stimulates a much greater phosphorylation of the FcR gamma -chain and subsequent downstream responses relative to CRP and collagen, presumably because of its ability to cause a greater degree of cross-linking of GPVI, The adapter LAT appears to play a critical role in recruiting a number of other adapter proteins to the surface membrane in response to activation of GPVI, presumably at sites of glycolipid-enriched microdomains, enabling an organized signaling cascade that leads to platelet activation.

关键词：衔接蛋白质类信号转导血小板/药物作用血小板/代谢载体蛋白质类/生理学胶原/药理学响尾蛇毒液类/药理学环AMP受体蛋白质/药理学 GRB2衔接蛋白质整合素类/代谢细胞内信号肽和蛋白质类外源凝集素类 C型膜蛋白质类磷蛋白类/生理学磷酰化蛋白质类/生理学受体胶原受体 IgG/生理学 C型磷脂酶类/生理学人类

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Structural and functional characterization of platelet receptor-mediated factor VIII binding

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第17期275卷 13071-13081页

作者： Ahmad, SS Scandura, JM Walsh, PN Temple Univ Sch Med Sol Sherry Thrombosis Res Ctr Philadelphia PA 19140 USA Temple Univ Sch Med Dept Biochem Philadelphia PA 19140 USA Temple Univ Sch Med Dept Med Philadelphia PA 19140 USA

Optimal. rates of factor X (FX) activation require occupancy of receptors for factor IXa (FIXa), factor VIII (FVIII), and FX on the activated platelet surface, The presence of FVIII and FX increases 5-fold the affinity of FIXa for the surface of activated platelets, and the presence of FVIII or FVIIIa generates a high affinity, low capacity specific FX-binding site on activated platelets. We have now examined the effects of FX and active site-inhibited FIXa (EGR-FIXa) on the binding of both FVIII and FVIIIa to activated platelets and show the following: (a) von Willebrand factor inhibits FVIII binding (K-i = 0.54 nw) but not FVIIIa binding;(b) thrombin and the thrombin receptor activation peptide (SFLLRN amide) are the most potent agonists required for FVIII-binding site expression, whereas ADP is inert;(c) FVa does not compete with FVIIIa or FVIII for functional platelet-binding sites;and (d) Annexin V is a potent inhibitor of FVIIIa binding (IC50 = 10 nM) to activated platelets. The A2 domain of FVIII significantly increases the affinity and stoichiometry of FVIIIa binding to platelets and contributes to the stability of the FX-activating complex, Both FVIII and FVIIIa binding were specific, saturable, and reversible. FVIII binds to specific, high affinity receptors on activated platelets (n = 484 +/- 59;K-d = 3.7 +/- 0.31 nM) and FVIIIa interacts with an additional 300-500 sites per platelet with enhanced affinity (K-d = 1.5 +/- 0.11 nM). FVIIIa binding to activated platelets in the presence of FIXa and FX is closely coupled with rates of F-X activation. The presence of EGR-FIXa and FX increases both the number and the affinity of binding sites on activated platelets for both FVIII and FVIIIa, emphasizing the validity of a three-receptor model in the assembly of the F-X-activating complex on the platelet surface.

关键词：膜联蛋白A5/代谢结合部位结合竞争性血小板/代谢剂量效应关系药物电泳聚丙烯酰氨凝胶因子Ⅸa/代谢因子Ⅷ/化学因子Ⅷ/代谢因子Ⅷa/化学因子Ⅷa/代谢因子Ⅴa/代谢因子Ⅹ/代谢蛋白质结合蛋白质结构三级 vonWillebrand因子/代谢人类

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Physical proximity and functional association of glycoprotein 1bα and protein-disulfide isomerase on the platelet plasma membrane

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第13期275卷 9758-9766页

作者： Burgess, JK Hotchkiss, KA Suter, C Dudman, NPB Szöllösi, J Chesterman, CN Chong, BH Hogg, PJ Univ New S Wales Sch Pathol Ctr Thrombosis & Vasc Res Sydney NSW 2052 Australia Prince Wales Hosp Dept Haematol Sydney NSW 2052 Australia St Vincents Hosp Garvan Inst Med Res Dept Mol & Cellular Oncol Darlinghurst NSW 2010 Australia Prince Henry Hosp Dept Cardiovasc Med Little Bay NSW 2036 Australia Univ Debrecen Dept Biophys & Cell Biol H-4012 Debrecen Hungary

Platelet function is influenced by the platelet thiol-disulfide balance. Platelet activation resulted in 440% increase in surface protein thiol groups. Two proteins that presented free thiol(s) on the activated platelet surface were protein-disulfide isomerase (PDI) and glycoprotein 1b alpha (GP1b alpha), PDI contains two active site dithiols/disulfides. The active sites of 26% of the PDI on resting platelets was in the dithiol form, compared with 81% in the dithiol form on activated platelets. Similarly, GP1b alpha presented one or more free thiols on the activated platelet surface but not on resting platelets. Anti-PDI antibodies increased the dissociation constant for binding of vWF to platelets by similar to 50% and PDI and GP1b alpha were sufficiently close on the platelet surface to allow fluorescence resonance energy transfer between chromophores attached to PDI and GP1b alpha. Incubation of resting platelets with anti-PDI antibodies followed by activation with thrombin enhanced labeling and binding of monoclonal antibodies to the N-terminal region of GP1b alpha on the activated platelet surface. These observations indicated that platelet activation triggered reduction of the active site disulfides of PDI and a conformational change in GP1b alpha that resulted in exposure of a free thiol(s).

关键词：抗体/免疫学血小板/酶学血小板/代谢细胞膜/酶学细胞膜/代谢分子量血小板活化血小板聚集血小板膜糖蛋白类/代谢蛋白质二硫化物异构酶类/血液蛋白质二硫化物异构酶类/免疫学巯基化合物/血液巯基化合物/化学 vonWillebrand因子/代谢人类

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Arachidonic acid in platelet microparticles up-regulates cyclooxygenase-2-dependent prostaglandin formation via a protein kinase C mitogen-activated protein kinase-dependent pathway

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第11期274卷 7545-7556页

作者： Barry, OP Kazanietz, MG Praticò, D FitzGerald, GA Univ Penn Sch Med Ctr Expt Therapeut Stellar Chance Labs 905 Philadelphia PA 19104 USA

Activation of platelets results in shedding of membrane microparticles (RIP) with potentially bioactive properties. Platelet MP modulate platelet, monocyte, and vascular endothelial cell function, both by direct effects of MP arachidonic acid (AA) and by its metabolism to bioactive prostanoids. We have previously reported that platelet MP induce expression of cyclooxygenase (COX)-2 and prostacyclin production in monocytes and endothelial cells. To elucidate further the molecular mechanisms that underlie RIP-induced upregulation of COX-2 expression, we investigated the response of a human monocytoid (U-937) cell line to platelet MP stimulation, In U-937 cells, RIP-induced COX-2 expression and eicosanoid formation is prevented by pharmacological inhibitors of protein kinase C (PKC), PI 3-kinase, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase, and p38 kinase, Treatment with the PI 3-kinase inhibitors wortmannin and LY294002 also blocked RIP-induced p42/p44 MAPK, p38, and JNK1 phosphorylation. Conversely, platelet RIP stimulation of U-937 cells results in direct activation of PKC, p42/p44 MAPK, p38 kinase, and c-Jun N-terminal kinase (JNK) as well as activation of the transcription factors c-Jun and Elk-l, However, MP failed to activate the cAMP response element. Activation of U-937 cells by MP induces translocation of classical (PKC beta), novel (PKC delta) and atypical (PKC zeta and PKC lambda) isozymes of PKC from the cytosol to the membrane, with concomitant activation of downstream MAPK. While RIP-induced activation of p42/p44 MAPK and p38 kinase is transient, a sustained activation of JNK1 was observed. Although PKC activation is required for RIP-induced p42/p44 MAPK, activation of the stress kinases p38 and JNK1 was PKC-independent, The fatty acid fraction of the MP accounted for these effects, which were mimicked by MP Ak Rather than acting directly via nuclear receptors, MP AA activates COX-2-dependent prostaglandin production by

关键词：花生四烯酸/生理学血小板/代谢钙-钙调素依赖性蛋白激酶类/代谢环氧化酶2 酶诱导同工酶类/生物合成同工酶类/代谢膜蛋白质类前列腺素内过氧化物合酶类/生物合成前列腺素内过氧化物合酶类/代谢前列腺素/生物合成蛋白激酶C/代谢信号传导 U937细胞增量调节/生理学人类

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Activation of the GP IIb-IIIa complex induced by platelet adhesion to collagen is mediated by both α₂β₁ integrin and GP VI

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第17期274卷 11897-11903页

作者： Nakamura, T Kambayashi, J Okuma, M Tandon, NN Otsuka Amer Pharmaceut Inc Maryland Res Labs Rockville MD 20850 USA Takashima Gen Hosp Shiga 5201121 Japan

alpha(2)beta(1) integrin, CD36, and GP VI have all been implicated in platelet-collagen adhesive interactions. We have investigated the role of these glycoproteins on activation of the GP IIb-IIIa complex induced by platelet adhesion to type I fibrillar and monomeric collagen under static conditions. In the presence of Mg2+, platelet adhesion to fibrillar collagen induced activation of the GP IIb-IIIa complex and complete spreading. Anti-alpha(2)beta(1) integrin and anti-GP VI antibodies inhibited the activation of the GP IIb-IIIa complex by about 40 and 50%, respectively, at 60 min although minimal inhibitory effects on adhesion were seen. Platelet spreading was markedly reduced by anti-alpha(2)beta(1) integrin antibody. The combination of anti-alpha(2)beta(1) integrin with anti-GP VI anti body completely inhibited both platelet adhesion and activation of the GP IIb-IIIa complex. Anti-CD36 antibody had no significant effects on platelet adhesion, spreading, and the activation of the GP IIb-IIIa complex at 60 min. Aspirin and the thromboxane A(2) receptor antagonist SQ29548 inhibited activation of the GP IIb-IIIa complex about 30% but had minimal inhibitory effect on adhesion. In the absence of Mg2+, there was significant activation of the GP IIb-IIIa complex brat minimal spreading was observed. Anti-GP VI antibody completely inhibited adhesion whereas no effect was observed with anti-alpha(2)beta(1) integrin antibody. Anti-CD36 antibody partially inhibited both adhesion and the activation of the GP IIb-IIIa complex. Platelet adhesion to monomeric collagen, which requires Mg2+ and is exclusively mediated by alpha(2)beta(1) integrin, resulted in partial activation of the GPIIb-IIIa complex and spreading. No significant effects were observed by anti-CD36 and anti-GP VI antibodies. These results suggest that both alpha(2)beta(1) integrin and GP VI are involved in inside-out signaling leading to activation of the GP IIb-IIIa complex after platelet adhesion to collagen a

关键词：抗体/代谢阿司匹林/药理学血小板/细胞学血小板/代谢细胞黏附/药物作用胶原/代谢马整合素类/拮抗剂和抑制剂整合素类/代谢血小板糖蛋白GPⅡb-Ⅲa复合物/代谢血小板膜糖蛋白类/拮抗剂和抑制剂血小板膜糖蛋白类/代谢受体胶原动物人类

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Ca²⁺ release and heat production by the endoplasmic reticulum Ca²⁺-ATPase of blood platelets -: Effect of the platelet activating factor

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第40期274卷 28344-28350页

作者： Mitidieri, F de Meis, L Univ Fed Rio de Janeiro Inst Ciencias Biomed Dept Bioquim Med BR-21941590 Rio De Janeiro Brazil

Different sarco/endoplasmic reticulum Ca2+-ATPases isoforms are found in blood platelets and in skeletal muscle. The amount of heat produced during ATP hydrolysis by vesicles derived from the endoplasmic reticulum of blood platelets was the same in the absence and presence of a transmembrane Ca2+ gradient. Addition of platelets activating factor (PAF) to the medium promoted both a Ca2+ efflux that was arrested by thapsigargin and an increase of the yield of heat produced during ATP hydrolysis. The calorimetric enthalpy of ATP hydrolysis (Delta H-cal) measured during Ca2+ transport varied between -10 and -12 kcal/mol without PAF and between -20 and -24 kcal/mol with 4 mu M PAF. Different from platelets, in skeletal muscle vesicles a thapsigargin-sensitive Ca2+ efflux and a high heat production during ATP hydrolysis were measured without PAF and the Delta H-cal varied between -10 and -12 kcal/mol in the absence of Ca2+ and between -22 up to -32 kcal/mol after formation of a transmembrane Ca2+ gradient. PAF did not enhance the rate of thapsigargin-sensitive Ca2+ efflux nor increase the yield of heat produced during ATP hydrolysis. These findings indicate that the platelets of Ca2+-ATPase isoforms are only able to convert osmotic energy into heat in the presence of PAF.

关键词：腺苷三磷酸/代谢血小板/药物作用血小板/酶学血小板/代谢钙/代谢钙转运ATP酶类/血液内质网/酶学热温度水解作用肌骨骼/代谢血小板活化因子/药理学动物人类兔

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EFFECTS OF FASTING ON PLASMA AND PLATELET-FREE FATTY-ACIDS AND PLATELET-FUNCTION IN HEALTHY MALES

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THROMBOSIS AND HAEMOSTASIS 1976年第2期36卷 325-333页

作者： GJESDAL, K NORDOY, A WANG, H BERNTSEN, H MJOS, OD INST CLIN MED DEPT INTERN MEDTROMSONORWAY UNIV TROMSO INST MED BIOLPHYSIOL SECTN-9012 TROMSONORWAY

10 healthy male volunteers fasted for 72 hours. Their plasma concentration of free fatty acid increased more than two-fold, to 1.8 mmol/1. The number of reversible venous “in vivo” platelet aggregates increased significantly (p <0.01); this figure correlated with the concentration of long-chain saturated free fatty acid in plasma (p <0.02). The correlation with the amount of long-chain saturated free fatty acid plus oleic acid (18:1) was even better (p <0.01). Plasma PF-4 concentration increased, suggesting increased platelet release reaction. In spite of the plasma increase, total platelet FFA concentration was reduced and there was a change in the distribution of platelet free fatty acid which correlated with the degree of aggregation.

关键词：血小板/代谢血小板/生理学禁食脂肪酸类非酯化/血液血小板聚集血小板因子4/分析绝食/血液成年人人类男(雄)性

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Purification, cloning, expression, and mechanism of action of a novel platelet aggregation inhibitor from the salivary gland of the blood-sucking bug, Rhodnius prolixus

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第17期275卷 12639-12650页

作者： Francischetti, IMB Ribeiro, JMC Champagne, D Andersen, J NIAID Parasit Dis Lab NIH Bethesda MD 20892 USA Univ Georgia Dept Entomol Athens GA 30602 USA Univ Arizona Dept Biochem Tucson AZ 85721 USA

Rhodnius prolixus aggregation inhibitor 1 (RPAI-1), a 19-kDa protein isolated from the salivary gland of R. prolixus was purified by strong cation exchange and reverse-phase high performance liquid chromatographies. Based on 49 amino-terminal amino acid sequences of RPAI-1, primers were produced to generate probes to screen an R. prolixus salivary gland cDNA library. A phage containing the full-length clone of RPAI-1 codes for a mature protein of 155 amino acids. RPAI-1 shows sequence homology to triabin and pallidipin, lipocalins from Triatoma pallidipennis. The cDNA sequence was cloned in Petl17B Escherichia coli expression vector, producing an active peptide. RPAI-1 inhibits human platelet-rich plasma aggregation triggered by low concentrations of ADP, collagen, arachidonic acid, thromboxane A(2) mimetics (U46619), and very low doses of thrombin and convulxin. Here we show that ADP is the target of RPAI-1 since (i) RPAI-1 inhibits ADP-dependent large aggregation formation and secretion triggered by U46619, without affecting Ca2+ increase and shape change;(ii) ADP restored the inhibition of U46619-induced platelet aggregation by RPAI-1, (iii) PGE(1)-induced increase of cAMP (which is antagonized by U46619 in an ADP-dependent manner) was restored by RPAI-1, (iv) RPAI-1 inhibits low concentrations of ADP-mediated responses of indomethacin-treated platelets, and (v) RPAI-1 binds to ADP, as assessed by large zone chromatography. RPAI-1 affects neither integrin alpha(2)beta(1)- nor glycoprotein VI-mediated platelet responses. We conclude that RPAI-1 is the first lipocalin described that inhibits platelet aggregation by a novel mechanism, binding to ADP.

关键词：腺苷二磷酸/代谢氨基酸序列花生四烯酸/代谢血小板/代谢钙/代谢细胞黏附细胞集合/药物作用色谱法高压液相色谱法离子交换克隆分子胶原/代谢响尾蛇毒液类/代谢环AMP/代谢 DNA 互补/代谢剂量效应关系药物昆虫蛋白质类外源凝集素类 C型分子序列数据血小板聚集抑制剂/代谢血小板聚集抑制剂/药代动力学红猎蝽属/化学红猎蝽属/遗传学涎腺/化学唾液蛋白质类和肽类/化学唾液蛋白质类和肽类/遗传学唾液蛋白质类和肽类/代谢序列同源性氨基酸血栓烷A2/药理学时间因素色氨酸/代谢动物牛人类兔

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Proteolytically activated receptor-3 - A member of an emerging gene family of protease receptors expressed on vascular endothelial cells and platelets

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TRENDS IN CARDIOVASCULAR MEDICINE 1999年第1-2期9卷 42-48页

作者： Cupit, LD Schmidt, VA Bahou, WF SUNY Stony Brook Dept Med Stony Brook NY 11794 USA Amer Heart Assoc Dallas TX 75231 USA SUNY Stony Brook Genet Program Stony Brook NY 11794 USA

Macromolecular assembly and generation of serine proteases on cellular surfaces is critically involved in regulation of hemostatic, inflammatory, or fibrinolytic pathways. The concept that a number of these serine proteases may effect cellular activation and proliferative responses has engendered an emerging paradigm focusing on the molecular mechanisms regulating cellular/protease interactions. Previous data suggest that some of these cellular responses are mediated by a novel class of G protein-coupled proteolytically activated receptors. Proteolytically activated receptor-3 (PAR-3) is the third member of this vapidly emerging gene family, all three of which (PAR-I, PAR-2, PAR-3) are known to co-cluster in the human genome, an are expressed on vascular endothelial cells, cells which critically regulate the hemostatic repertoire. This review will focus on the genetics of these receptors (emphasizing recent advances in the identification and characterization of PAR-3), review known structure/function similarities, and outline potential links in regulation of the hemostatic response by protease generation on the endothelial cell surface. (C) 1999, Elsevier Science Inc.

关键词：血小板/代谢内皮血管/代谢纤维蛋白溶解/生理学 GTP结合蛋白质类/生理学基因表达调控基因表达调控酶学止血/生理学炎症/病理生理学大分子物质受体细胞表面/遗传学受体细胞表面/生理学受体凝血酶/遗传学受体凝血酶/生理学丝氨酸内肽酶类/遗传学丝氨酸内肽酶类/生理学构效关系动物人类小鼠

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