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Journal articles on the topic 'Platelet factor 4'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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1

Shimizu, T., Y. Ishikawa, Y. Morishima, T. Fukuda, and K. Kato. "Platelet factor 4 release from the platelets stored in platelet concentrates." Transfusion 25, no. 5 (September 1985): 420–23. http://dx.doi.org/10.1046/j.1537-2995.1985.25586020114.x.

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2

CAPITANIO, A., S. NIEWIAROWSKI, B. RUCINSKI, G. TUSZYNSKI, C. CIERNIEWSKI, D. HERSHOCK, and E. KORNECKI. "Interaction of platelet factor 4 with human platelets." Biochimica et Biophysica Acta (BBA) - General Subjects 839, no. 2 (April 17, 1985): 161–73. http://dx.doi.org/10.1016/0304-4165(85)90033-9.

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3

O'Brien, J. R. "PLATELET FACTOR 4 (PF 4) AND THE PLATELET MEMBRANE." Acta Medica Scandinavica 191, S525 (April 24, 2009): 65–66. http://dx.doi.org/10.1111/j.0954-6820.1972.tb05793.x.

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4

Sottile, Jane, Deane F. Mosher, Jan Fullenweider, and James N. George. "Human Platelets Contain mRNA Transcripts for Platelet Factor 4 and Actin." Thrombosis and Haemostasis 62, no. 04 (1989): 1100–1102. http://dx.doi.org/10.1055/s-0038-1647125.

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SummaryRNAs from a number of cells, including platelets, were analyzed by Northern blotting for the presence of transcripts to four platelet proteins - actin, thrombospondin, fibronectin, and platelet factor 4. RNA from platelets contains considerable amounts of mRNA for platelet factor 4, easily detectable mRNA for actin, and traces of mRNA for thrombospondin. mRNA for platelet factor 4 was not detected in human lymphocytes or in any of 5 human cell lines.

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5

Cowan, S. W., E. N. Bakshi, K. J. Machin, and N. W. Isaacs. "Binding of heparin to human platelet factor 4." Biochemical Journal 234, no. 2 (March 1, 1986): 485–88. http://dx.doi.org/10.1042/bj2340485.

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Platelet factor 4 is a small protein (Mr 7756) from the alpha-granules of blood platelets which binds strongly to and neutralizes the anticoagulant properties of heparin. From an analysis of X-ray crystallographic data a model for the binding of platelet factor 4 to heparin is proposed.

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6

Dickhout, Annemiek, Bibian M. E. Tullemans, Johan W. M. Heemskerk, Victor L. J. L. Thijssen, Marijke J. E. Kuijpers, and Rory R. Koenen. "Galectin-1 and platelet factor 4 (CXCL4) induce complementary platelet responses in vitro." PLOS ONE 16, no. 1 (January 7, 2021): e0244736. http://dx.doi.org/10.1371/journal.pone.0244736.

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Galectin-1 (gal-1) is a carbohydrate-binding lectin with important functions in angiogenesis, immune response, hemostasis and inflammation. Comparable functions are exerted by platelet factor 4 (CXCL4), a chemokine stored in the α-granules of platelets. Previously, gal-1 was found to activate platelets through integrin αIIbβ3. Both gal-1 and CXCL4 have high affinities for polysaccharides, and thus may mutually influence their functions. The aim of this study was to investigate a possible synergism of gal-1 and CXCL4 in platelet activation. Platelets were treated with increasing concentrations

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7

Day, H. James, H. Stormorken, and H. Holmsen. "Subcellular Localization of Platelet Factor 3 and Platelet Factor 4." Scandinavian Journal of Haematology 10, no. 4 (April 24, 2009): 254–60. http://dx.doi.org/10.1111/j.1600-0609.1973.tb00069.x.

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8

Leavitt, Andrew D. "What for platelet factor 4?" Blood 110, no. 4 (August 15, 2007): 1090. http://dx.doi.org/10.1182/blood-2007-05-091363.

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9

Robinson, C. "Recombinant Human Platelet Factor 4." Drugs of the Future 20, no. 2 (1995): 148. http://dx.doi.org/10.1358/dof.1995.020.02.284334.

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10

Lorenz, R., and M. Brauer. "Platelet factor 4 (PF 4) in septicaemia." Infection 16, no. 5 (September 1988): 273–76. http://dx.doi.org/10.1007/bf01645070.

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11

Gjesdal, K., and A. F. Abrahamsen. "Platelet Consumption and Plasma Concentration of Platelet Factor 4 (PF-4)." Scandinavian Journal of Haematology 17, no. 1 (April 24, 2009): 5–9. http://dx.doi.org/10.1111/j.1600-0609.1976.tb02834.x.

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12

O'Brien, J. R. "PLATELET FACTOR 3 (PF 3) AND PLATELET FACTOR 4 (PF 4) AS A GUIDE TO PLATELET MEMBRANE STRUCTURE." Acta Medica Scandinavica 191, S525 (April 24, 2009): 87–88. http://dx.doi.org/10.1111/j.0954-6820.1972.tb05799.x.

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13

Levine, SP, LK Knieriem, and MA Rager. "Platelet factor 4 and the platelet secreted proteoglycan: immunologic characterization by crossed immunoelectrophoresis." Blood 75, no. 4 (February 15, 1990): 902–10. http://dx.doi.org/10.1182/blood.v75.4.902.902.

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Abstract Platelet factor 4 (PF4) is a hydrophobic, alpha-granule protein with potent antiheparin activity. It also binds to a chondroitin sulfate- containing proteoglycan (PG) isolated from platelets. In order to evaluate further the relationship between PF4 and the chondroitin sulfate-containing proteoglycan in resting platelets, the PF4-binding proteoglycan from human platelets has been purified using purified PF4 as an affinity ligand and used to prepare polyclonal antiserum. Two antisera have been characterized: one reacts primarily with chondroitin sulfate (CS), the other reacts with the

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14

Levine, SP, LK Knieriem, and MA Rager. "Platelet factor 4 and the platelet secreted proteoglycan: immunologic characterization by crossed immunoelectrophoresis." Blood 75, no. 4 (February 15, 1990): 902–10. http://dx.doi.org/10.1182/blood.v75.4.902.bloodjournal754902.

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Platelet factor 4 (PF4) is a hydrophobic, alpha-granule protein with potent antiheparin activity. It also binds to a chondroitin sulfate- containing proteoglycan (PG) isolated from platelets. In order to evaluate further the relationship between PF4 and the chondroitin sulfate-containing proteoglycan in resting platelets, the PF4-binding proteoglycan from human platelets has been purified using purified PF4 as an affinity ligand and used to prepare polyclonal antiserum. Two antisera have been characterized: one reacts primarily with chondroitin sulfate (CS), the other reacts with the protein c

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15

Hayashi, Nobana, Junichi Chihara, Yohnosuke Kobayashi, Tomokazu Kakazu, Dai Kurachi, Takahiro Yamamoto, and Shigenori Nakajima. "Effect of Platelet-Activating Factor and Platelet Factor 4 on Eosinophil Adhesion." International Archives of Allergy and Immunology 104, no. 1 (1994): 57–59. http://dx.doi.org/10.1159/000236754.

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16

Ryo, Ryukichi, Mutsumi Yasunaga, Katsuyasu Saigo, and Nobuo Yamaguchi. "Megakaryocytic Leukemia and Platelet Factor 4." Leukemia & Lymphoma 8, no. 4-5 (January 1992): 327–36. http://dx.doi.org/10.3109/10428199209051011.

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17

Williams, R. Taylor, Lakshmi V. Damaraju, Mary Ann Mascelli, Elliot S. Barnathan, Robert M. Califf, Maarten L. Simoons, Efthymios N. Deliargyris, and David C. Sane. "Anti-Platelet Factor 4/Heparin Antibodies." Circulation 107, no. 18 (May 13, 2003): 2307–12. http://dx.doi.org/10.1161/01.cir.0000066696.57519.af.

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18

&NA;. "Rapid Heparin/Platelet Factor 4 Test." Nurse Practitioner 30, no. 1 (January 2005): 62. http://dx.doi.org/10.1097/00006205-200501000-00009.

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19

Mammen, Eberhard. "Platelet Factor 4 in Cardiovascular Disease." Seminars in Thrombosis and Hemostasis 30, no. 03 (July 29, 2004): 269–71. http://dx.doi.org/10.1055/s-2004-831038.

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20

Slungaard, Arne. "Platelet factor 4: a chemokine enigma." International Journal of Biochemistry & Cell Biology 37, no. 6 (June 2005): 1162–67. http://dx.doi.org/10.1016/j.biocel.2004.12.003.

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21

Villanueva, German B., Nancy Allen, and Daniel Walz. "Circular dichroism of platelet factor 4." Archives of Biochemistry and Biophysics 261, no. 1 (February 1988): 170–74. http://dx.doi.org/10.1016/0003-9861(88)90115-4.

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22

Chen, Jinhui, Gang Liu, Yan Hong, Jing Han, Zhe Yang, Yanping Yang, Hong Li, Shumin Wang, Lili Jue, and Qi Wang. "Regulation of Atherosclerosis by Toll-Like Receptor 4 Induced by Serum Amyloid 1: A Systematic In Vitro Study." BioMed Research International 2022 (September 15, 2022): 1–14. http://dx.doi.org/10.1155/2022/4887593.

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The objective of this study was to investigate the effects of serum amyloid 1 (SAA1) on activation of endothelial cells, formation of foam cells, platelet aggregation, and monocyte/platelet adhesion to endothelial cells. The effect of SAA1 on the inflammatory activation of endothelial cells was investigated by detecting the expression of inflammatory factors and adhesion molecules. The role of SAA1 in formation of foam cells was verified by detecting lipid deposition and expression of molecules related to the formation of foam cells. After platelets were stimulated by SAA1, the aggregation rat

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23

Campbell, Robert A., Thomas H. Fischer, and Alisa S. Wolberg. "Rehydrated, Lyophilized Platelets Generate Thrombin in the Presence of Recombinant Factor VIIa." Blood 106, no. 11 (November 16, 2005): 4057. http://dx.doi.org/10.1182/blood.v106.11.4057.4057.

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Abstract The anti-bleeding therapy, recombinant factor VIIa (rFVIIa), is thought to bind to the platelet’s surface and increase thrombin generation in hemophilia. However, high plasma levels of rFVIIa are required, in part, due to the weak binding of rFVIIa to platelets. We hypothesized that the efficacy of the therapy could be improved by administering rFVIIa already bound to platelets. A recently described protocol involving pretreatment of platelets with paraformaldehyde permits platelets to be lyophilized while preserving many platelet functions. Such platelets could be used for binding rF

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24

Ren, Qiansheng, Christian Wimmer, Michael C. Chicka, Shaojing Ye, Yi Ren, Frederick M. Hughson, and Sidney W. Whiteheart. "Munc13-4 is a limiting factor in the pathway required for platelet granule release and hemostasis." Blood 116, no. 6 (August 12, 2010): 869–77. http://dx.doi.org/10.1182/blood-2010-02-270934.

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Abstract Activation-dependent platelet granule release is mediated by integral membrane proteins called soluble N-ethylmaleimide–sensitive fusion protein attachment protein receptors (SNAREs) and their regulators; however, the mechanisms for this process are ill-defined. To further characterize platelet secretion, we analyzed the function of platelets from Unc13dJinx mice. Platelets from these animals lack the putative vesicle priming factor, Munc13-4, and have a severe secretion defect. Release from dense granules was completely ablated and that from α-granules and lysosomes was severely comp

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25

Haselton, F. R., and J. S. Alexander. "Platelets and a platelet-released factor enhance endothelial barrier." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 6 (December 1, 1992): L670—L678. http://dx.doi.org/10.1152/ajplung.1992.263.6.l670.

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The role of platelets in the maintenance of endothelial barrier is examined in an in vitro model of the microvasculature. Human platelets (6,000/microliters) perfused through a cell column of endothelial-covered microcarriers decrease paracellular permeability of sodium fluorescein (mol wt 342) to 63% of baseline values. This effect is reversible and a second application and removal of platelets produces a similar response. This effect occurs within 5 min and reverses within 10 min after platelet removal. The reduction in permeability is not due to mechanical obstruction of endothelial junctio

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26

Barnes, J. L., K. A. Woodruff, S. P. Levine, and H. E. Abboud. "Inhibition of mesangial cell proliferation by platelet factor 4." Journal of the American Society of Nephrology 7, no. 7 (July 1996): 991–98. http://dx.doi.org/10.1681/asn.v77991.

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Platelet factor 4(PF4), an abundant platelet secretory product, is a strong candidate for modulating glomerular pathology. Because PF4 might be released from platelets and influence intrinsic cell growth during glomerular injury, the effect of PF4 on fetal calf serum- and platelet-derived growth factor (PDGF)-induced mesangial cell mitogenesis was examined. Mitogenesis was measured as the amount of 3H-thymidine incorporated into acid-precipitable material as well as by autoradiography. The effect of PF4 on mesangial cell expression of mRNA for PDGF A chain and transforming growth factor-beta (

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27

Jayachandran, Muthuvel, Antonio Sanzo, Whyte G. Owen, and Virginia M. Miller. "Estrogenic regulation of tissue factor and tissue factor pathway inhibitor in platelets." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H1908—H1916. http://dx.doi.org/10.1152/ajpheart.01292.2004.

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Oral estrogen treatment increases thrombotic risk. Tissue factor (TF), tissue factor pathway inhibitor (TFPI), and platelet interaction with leukocytes are important determinants of thrombogenesis. Therefore, the present study was designed to define and compare platelet TF and TFPI mRNA and adhesion protein expression in platelets derived from animals treated with different types of oral estrogens. Ovariectomized pigs were treated with 17β-estradiol (2 mg/day), conjugated equine estrogen (CEE; 0.625 mg/day), or raloxifene (60 mg/day) for 4 wk. Compared with intact animals, ovariectomy and trea

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28

Uhlin-Hansen, L., D. Langvoll, T. Wik, and SO Kolset. "Blood platelets stimulate the expression of chondroitin sulfate proteoglycan in human monocytes." Blood 80, no. 4 (August 15, 1992): 1058–65. http://dx.doi.org/10.1182/blood.v80.4.1058.1058.

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Abstract Mononuclear phagocytes synthesize chondroitin sulfate proteoglycan (CSPG), which is constitutively secreted. Because mononuclear phagocytes are known to interact with blood platelets, the effect of platelets on the release of CSPG in cultured human monocytes was investigated. After 6 days in vitro, the monocytes were supplied with fresh medium with different additions and subsequently exposed to [35S]sulfate for 24 hours before the medium fractions were harvested and analyzed for content of [35S]CSPG. Indirect evidence for the release of stimulatory factors from blood platelets was fo

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29

Uhlin-Hansen, L., D. Langvoll, T. Wik, and SO Kolset. "Blood platelets stimulate the expression of chondroitin sulfate proteoglycan in human monocytes." Blood 80, no. 4 (August 15, 1992): 1058–65. http://dx.doi.org/10.1182/blood.v80.4.1058.bloodjournal8041058.

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Mononuclear phagocytes synthesize chondroitin sulfate proteoglycan (CSPG), which is constitutively secreted. Because mononuclear phagocytes are known to interact with blood platelets, the effect of platelets on the release of CSPG in cultured human monocytes was investigated. After 6 days in vitro, the monocytes were supplied with fresh medium with different additions and subsequently exposed to [35S]sulfate for 24 hours before the medium fractions were harvested and analyzed for content of [35S]CSPG. Indirect evidence for the release of stimulatory factors from blood platelets was found when

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30

Theilmeier, Gregor, Carine Michiels, Erik Spaepen, Ingrid Vreys, Désiré Collen, Jos Vermylen, and Marc F. Hoylaerts. "Endothelial von Willebrand factor recruits platelets to atherosclerosis-prone sites in response to hypercholesterolemia." Blood 99, no. 12 (June 15, 2002): 4486–93. http://dx.doi.org/10.1182/blood.v99.12.4486.

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Platelets are thought to play a causal role during atherogenesis. Platelet-endothelial interactions in vivo and their molecular mechanisms under shear are, however, incompletely characterized. Here, an in vivo platelet homing assay was used in hypercholesterolemic rabbits to track platelet adhesion to plaque predilection sites. The role of platelet versus aortic endothelial cell (EC) activation was studied in an ex vivo flow chamber. Pathways of human platelet immobilization were detailed during in vitro perfusion studies. In rabbits, a 0.125% cholesterol diet induced no lesions within 3 month

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31

Krauel, Krystin, Nikolay Medvedev, Raghavendra Palankar, Andreas Greinacher, and Mihaela Delcea. "Micropatterned array to assess the interaction of single platelets with platelet factor 4-heparin-IgG complexes." Thrombosis and Haemostasis 111, no. 05 (2014): 862–72. http://dx.doi.org/10.1160/th13-09-0752.

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SummaryWe report a strategy to generate by electron beam lithography high fidelity micropatterned arrays to assess the interaction of single platelets with immobilised ligands. As a proof-of-principle we functionalised the microarrays with platelet factor 4 (PF4)-heparin-IgG complexes. We embedded biotinylated water-soluble quantum dots into polyethylene glycol (PEG)-coated micropatterned arrays and functionalised them via streptavidin to bind biotinylated ligands, here biotinylated-PF4/heparin complexes. The integrity of the PF4/heparin-complexes was shown by binding of anti-PF4/heparin antib

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32

Cines, Douglas B., Serge V. Yarovoi, Sergei V. Zaitsev, Tatiana Lebedeva, Lubica Rauova, Mortimer Poncz, Gowthami M. Arepally, et al. "Polyphosphate/platelet factor 4 complexes can mediate heparin-independent platelet activation in heparin-induced thrombocytopenia." Blood Advances 1, no. 1 (November 22, 2016): 62–74. http://dx.doi.org/10.1182/bloodadvances.2016000877.

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Key Points Polyphosphates form antigenic complexes with PF4 that are recognized by HIT antibodies. Polyphosphate/PF4 complexes released by activated platelets can mediate platelet aggregation by HIT antibodies in the absence of heparin or cell-surface chondroitin sulfate.

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33

Baruch, Dominique, Theo Lindhout, Evelyne Dupuy, and Jacques P. Caen. "Thrombin-Induced Platelet Factor Va Formation in Patients with a Gray Platelet Syndrome." Thrombosis and Haemostasis 58, no. 02 (1987): 768–71. http://dx.doi.org/10.1055/s-0038-1645967.

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SummaryThe present study was initiated to establish the functional factor V concentration in platelets of patients with a mild bleeding disorder ascribed to a gray platelet syndrome. This inherited platelet disorder has been characterized by a specific deficiency of alpha-granules and subsequent deficiencies in the alpha-granule proteins. We found that the concentration of plasma factor V was slightly decreased (70% of normal values). In contrast, platelet factor Va formation was severely impaired. Besides a much lower factor V content than in control platelets (10-20% of normal), the dependen

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34

&NA;. "Platelet factor-4 reverses effects of heparin." Inpharma Weekly &NA;, no. 1064 (November 1996): 12. http://dx.doi.org/10.2165/00128413-199610640-00027.

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35

&NA;. "Platelet factor-4 reverses heparin-induced anticoagulation." Inpharma Weekly &NA;, no. 989 (June 1995): 11. http://dx.doi.org/10.2165/00128413-199509890-00022.

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36

Mixon, Timothy, and Gregory Dehmer. "Recombinant Platelet Factor 4 for Heparin Neutralization." Seminars in Thrombosis and Hemostasis 30, no. 03 (July 29, 2004): 369–77. http://dx.doi.org/10.1055/s-2004-831050.

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37

Bikfalvi, Andreas. "Platelet Factor 4: An Inhibitor of Angiogenesis." Seminars in Thrombosis and Hemostasis 30, no. 03 (July 29, 2004): 379–85. http://dx.doi.org/10.1055/s-2004-831051.

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38

EIKA, C., and H. C. GODAL. "Inactivation of Platelet Factor 4 in Plasma." Scandinavian Journal of Haematology 9, no. 1-6 (April 24, 2009): 343–50. http://dx.doi.org/10.1111/j.1600-0609.1972.tb00951.x.

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39

Williams, R. D., T. E. Maione, K. E. Lynch, D. F. Keene, and M. N. DʼAmbra. "RECOMBINANT HUMAN PLATELET FACTOR 4 (r-PF4)." Anesthesiology 77, Supplement (September 1992): A158. http://dx.doi.org/10.1097/00000542-199209001-00158.

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40

Carr, Marcus E., Gilbert C. White, and Don A. Gabriel. "Platelet factor 4 enhances fibrin fiber polymerization." Thrombosis Research 45, no. 5 (March 1987): 539–43. http://dx.doi.org/10.1016/0049-3848(87)90316-1.

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41

Briquet-Laugier, V., C. Lavenu-Bombled, A. Schmitt, M. Leboeuf, G. Uzan, A. Dubart-Kupperschmitt, and J. P. Rosa. "Probing platelet factor 4 alpha-granule targeting." Journal of Thrombosis and Haemostasis 2, no. 12 (December 2004): 2231–40. http://dx.doi.org/10.1111/j.1538-7836.2004.01037.x.

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42

Thachil, Jecko. "The prothrombotic potential of platelet factor 4." European Journal of Internal Medicine 21, no. 2 (April 2010): 79–83. http://dx.doi.org/10.1016/j.ejim.2009.11.007.

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43

Smith, C. C. T., L. D. Curtis, A. P. Delamothe, B. N. C. Prichard, and D. J. Betteridge. "The Distribution of Catecholamines between Platelets and Plasma in Normal Human Subjects." Clinical Science 69, no. 1 (July 1, 1985): 1–6. http://dx.doi.org/10.1042/cs0690001.

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1. We have used high-performance liquid chromatography with electrochemical detection to measure content of adrenaline and noradrenaline in platelets in 13 normal subjects at rest. 2. Subjects were exercised to raise plasma catecholamine levels and promote the platelet release reaction. 3. There was a significant positive correlation between plasma noradrenaline concentrations and platelet noradrenaline content. 4. Platelet/plasma concentration ratios were 1855 for noradrenaline and 268 for adrenaline at rest and 473 and 152 respectively after exercise. 5. Plasma noradrenaline levels positivel

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44

Shigeta, Osamu, Weiqi Lu, John C. Holt, L. Henry Edmunds, and Stefan Niewiarowski. "Ovine platelet factor 4: Purification, amino acid sequence, radioimmunoassay and comparison with platelet factor 4 of other species." Thrombosis Research 64, no. 4 (November 1991): 509–20. http://dx.doi.org/10.1016/0049-3848(91)90351-v.

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45

Burgers, JA, RC Schweizer, L. Koenderman, PL Bruijnzeel, and JW Akkerman. "Human platelets secrete chemotactic activity for eosinophils." Blood 81, no. 1 (January 1, 1993): 49–55. http://dx.doi.org/10.1182/blood.v81.1.49.49.

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Abstract Thrombin-stimulated platelets liberate factors that induce chemotaxis of eosinophils and raise their cytosolic Ca2+ content ([Ca2+]i). The sources of this activity are the dense- and alpha-granules because inhibition of prostaglandin endoperoxide/thromboxane A2 formation and the platelet-activating factor receptor-antagonist WEB 2086 have no effect. Platelets from patients with Storage-Pool Deficiency show about 60% of the normal chemotactic activity with little effect on [Ca2+]i, whereas completely degranulated platelets fail to affect eosinophils. In concentrations secreted by the p

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46

Burgers, JA, RC Schweizer, L. Koenderman, PL Bruijnzeel, and JW Akkerman. "Human platelets secrete chemotactic activity for eosinophils." Blood 81, no. 1 (January 1, 1993): 49–55. http://dx.doi.org/10.1182/blood.v81.1.49.bloodjournal81149.

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Thrombin-stimulated platelets liberate factors that induce chemotaxis of eosinophils and raise their cytosolic Ca2+ content ([Ca2+]i). The sources of this activity are the dense- and alpha-granules because inhibition of prostaglandin endoperoxide/thromboxane A2 formation and the platelet-activating factor receptor-antagonist WEB 2086 have no effect. Platelets from patients with Storage-Pool Deficiency show about 60% of the normal chemotactic activity with little effect on [Ca2+]i, whereas completely degranulated platelets fail to affect eosinophils. In concentrations secreted by the platelets,

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47

Pitsilos, Stephanie, Jennifer Hunt, Emile Mohler, Anand Prabhakar, Mortimer Poncz, Jennine Dawicki, Tigran Khalapyan, et al. "Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters." Thrombosis and Haemostasis 90, no. 12 (2003): 1112–20. http://dx.doi.org/10.1160/th03-02-0069.

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SummaryEmerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistoc

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48

Kelton, JG, JW Smith, TE Warkentin, CP Hayward, GA Denomme, and P. Horsewood. "Immunoglobulin G from patients with heparin-induced thrombocytopenia binds to a complex of heparin and platelet factor 4." Blood 83, no. 11 (June 1, 1994): 3232–39. http://dx.doi.org/10.1182/blood.v83.11.3232.3232.

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Abstract Heparin-induced thrombocytopenia (HIT) is an important complication of heparin therapy. Although there is general agreement that platelet activation in vitro by the HIT IgG is mediated by the platelet Fc receptor, the interaction among the antibody, heparin, and platelet membrane components is uncertain and debated. In this report, we describe studies designed to address these interactions. We found, as others have noted, that a variety of other sulfated polysaccharides could substitute for heparin in the reaction. Using polysaccharides selected for both size and charge, we found that

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Kelton, JG, JW Smith, TE Warkentin, CP Hayward, GA Denomme, and P. Horsewood. "Immunoglobulin G from patients with heparin-induced thrombocytopenia binds to a complex of heparin and platelet factor 4." Blood 83, no. 11 (June 1, 1994): 3232–39. http://dx.doi.org/10.1182/blood.v83.11.3232.bloodjournal83113232.

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Abstract:

Heparin-induced thrombocytopenia (HIT) is an important complication of heparin therapy. Although there is general agreement that platelet activation in vitro by the HIT IgG is mediated by the platelet Fc receptor, the interaction among the antibody, heparin, and platelet membrane components is uncertain and debated. In this report, we describe studies designed to address these interactions. We found, as others have noted, that a variety of other sulfated polysaccharides could substitute for heparin in the reaction. Using polysaccharides selected for both size and charge, we found that reactivi

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Duckers, Connie, Paolo Simioni, Luca Spiezia, Claudia Radu, Paolo Dabrilli, Sabrina Gavasso, Jan Rosing, and Elisabetta Castoldi. "Residual platelet factor V ensures thrombin generation in patients with severe congenital factor V deficiency and mild bleeding symptoms." Blood 115, no. 4 (January 28, 2010): 879–86. http://dx.doi.org/10.1182/blood-2009-08-237719.

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Abstract:

Abstract Coagulation factor V (FV), present in plasma and platelets, is indispensable to thrombin formation, yet patients with undetectable plasma FV seldom experience major bleeding. We used thrombin generation assays to explore the role of platelet FV in 4 patients with severe congenital FV deficiency (3 with plasma FV clotting activity [FV:C] < 1%). When triggered with tissue factor (TF) concentrations up to 50pM, platelet-poor plasma (PPP) from the patients with undetectable plasma FV showed no thrombin generation, whereas platelet-rich plasma (PRP) formed thrombin already at 1 to 5pM o

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