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Artículos de revistas sobre el tema "Platelet activating factor"

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Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 31 de enero de 2023

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1

Perry, Seth W., Jason A. Hamilton, Larry W. Tjoelker, Ghassan Dbaibo, Kirk A. Dzenko, Leon G. Epstein, Yusuf Hannun, J. Steven Whittaker, Stephen Dewhurst y Harris A. Gelbard. "Platelet-activating Factor Receptor Activation". Journal of Biological Chemistry 273, n.º 28 (10 de julio de 1998): 17660–64. http://dx.doi.org/10.1074/jbc.273.28.17660.

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2

Zhou, W., M. A. Javors y M. S. Olson. "Platelet-activating factor as an intercellular signal in neutrophil-dependent platelet activation." Journal of Immunology 149, n.º 5 (1 de septiembre de 1992): 1763–69. http://dx.doi.org/10.4049/jimmunol.149.5.1763.

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Abstract The role of platelet-activating factor (PAF) in heterotypic cell to cell interactions in a rabbit neutrophil-platelet mixture model was investigated. Platelets were exposed to each of three chemotactic agonists: PAF, leukotriene B4 (LTB4), or FMLP. Only PAF stimulated aggregation, [3H]serotonin secretion, and cytosolic Ca2+ mobilization in platelets alone. However, platelets were stimulated by LTB4 and FMLP in the presence of neutrophils. This neutrophil-dependent platelet activation was blocked by pretreatment of platelets with PAF receptor antagonists, and was prevented by desensitization of platelets to PAF. Furthermore, the time-course of platelet activation showed a positive correlation with PAF production by neutrophils stimulated with either LTB4 or FMLP. The PAF-mediated neutrophil-platelet interaction was dependent on direct cell to cell contact, as demonstrated by experiments in which the majority of newly formed PAF was neutrophil associated (rather than released). Platelet activation did not occur when the neutrophil-platelet mixture was not stirred, minimizing cell to cell contact, or when platelets were challenged with a cell-free supernatant prepared from neutrophils activated with LTB4 or FMLP. Finally, the neutrophil-platelet interaction was abolished by SC-49992, a peptidomimetic of the fibrinogen binding sequence Arg-Gly-Asp-Phe, indicating a Arg-Gly-Asp-specific recognition mechanism. Our results demonstrate that neutrophil-generated PAF plays a crucial role in neutrophil-dependent platelet activation in this model system. This type of intercellular signaling event may be important in certain inflammatory or thrombotic processes.

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3

KAWASAKI, Tomio y Jun-ichi KAMBAYASHI. "Platelet-activating Factor". Japanese Journal of Thrombosis and Hemostasis 2, n.º 4 (1991): 274–85. http://dx.doi.org/10.2491/jjsth.2.274.

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4

Kingsnorth, A. N. "Platelet-Activating Factor". Scandinavian Journal of Gastroenterology 31, sup219 (enero de 1996): 28–31. http://dx.doi.org/10.3109/00365529609104996.

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5

McCORMACK, DAVID G., PETER J. BARNES y TIMOTHY W. EVANS. "Platelet-activating factor". Critical Care Medicine 18, n.º 12 (diciembre de 1990): 1398–402. http://dx.doi.org/10.1097/00003246-199012000-00018.

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6

Martin, John. "PLATELET-ACTIVATING FACTOR". Lancet 332, n.º 8626-8627 (diciembre de 1988): 1486. http://dx.doi.org/10.1016/s0140-6736(88)90956-7.

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7

Humphreys, Randy F. "PLATELET ACTIVATING FACTOR". Southern Medical Journal 83, Supplement (septiembre de 1990): 2S—2. http://dx.doi.org/10.1097/00007611-199009001-00004.

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8

Prescott, S. M., G. A. Zimmerman y T. M. McIntyre. "Platelet-activating factor." Journal of Biological Chemistry 265, n.º 29 (octubre de 1990): 17381–84. http://dx.doi.org/10.1016/s0021-9258(18)38167-5.

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9

Welch, Emily J., Ram P. Naikawadi, Zhenyu Li, Phoebe Lin, Satoshi Ishii, Takao Shimizu, Chinnaswamy Tiruppathi, Xiaoping Du, Papasani V. Subbaiah y Richard D. Ye. "Opposing Effects of Platelet-Activating Factor and Lyso-Platelet-Activating Factor on Neutrophil and Platelet Activation". Molecular Pharmacology 75, n.º 1 (17 de octubre de 2008): 227–34. http://dx.doi.org/10.1124/mol.108.051003.

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10

Lomazova, K. D., A. M. Polyakova, O. S. Astrina y D. B. Tsukerman. "Platelet activating factor and endotoxin-induced platelet activation". Bulletin of Experimental Biology and Medicine 107, n.º 5 (mayo de 1989): 611–14. http://dx.doi.org/10.1007/bf00841762.

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11

Wimberly, H. C., D. O. Slauson y N. R. Neilsen. "Functional and Biochemical Characterization of Immunologically Derived Equine Platelet-Activating Factor". Veterinary Pathology 22, n.º 4 (julio de 1985): 375–86. http://dx.doi.org/10.1177/030098588502200413.

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Antigen-specific challenge of equine leukocytes induced the non-lytic release of a platelet-activating factor in vitro. The equine platelet-activating factor stimulated the release of serotonin from equine platelets in a dose-responsive manner, independent of the presence of cyclo-oxygenase pathway inhibitors such as indomethacin. Rabbit platelets were also responsive to equine platelet-activating factor. The release of equine platelet-activating factor was a rapid reaction with near maximal secretion taking place in 30 seconds. Addition of equine platelet-activating factor to washed equine platelets stimulated platelet aggregation which could not be inhibited by the presence of aspirin or indomethacin. Platelets preincubated with equine platelet-activating factor became specifically desensitized to equine platelet-activating factor while remaining responsive to other platelet stimuli such as collagen and epinephrine. The following biochemical properties of equine platelet-activating factor are identical to those properties of 1-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC): stability upon exposure to air and acid; loss of functional activity after basecatalyzed methanolysis with subsequent acylation that returned all functional activity; and identical relative mobilities on silica gel G plates developed with chloroform:methanol:water (65:35:6, volume/volume). The combined functional and biochemical characteristics of equine platelet-activating factor strongly suggest identity between this naturally occurring, immunologically derived equine factor and AGEPC.

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12

Johnson, C. D. "Platelet-Activating Factor and Platelet-Activating Factor Antagonists in Acute Pancreatitis". Digestive Surgery 16, n.º 2 (1999): 93–101. http://dx.doi.org/10.1159/000018699.

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13

Yasuda, K., M. Takashima, K. Umesaki, S. Urakawa, T. Kamiya, S. Matsuoka, Y. Horikoshi, T. Nakajima y I. Sawaragi. "Platelet activating factor and platelet activating factor acetylhydrolase in uteroplacental circulation". Placenta 15, n.º 7 (octubre de 1994): A94. http://dx.doi.org/10.1016/0143-4004(94)90228-3.

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14

Summers, James B., Steven K. Davidsen y George S. Sheppard. "Platelet Activating Factor Antagonists". Current Pharmaceutical Design 1, n.º 2 (septiembre de 1995): 161–90. http://dx.doi.org/10.2174/1381612801666220917215816.

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Platelet Activating Factor (PAF) is a D-glycerol-derived phospholipid which is a potent endogenous mediator of inflammation. PAF is synthesized and released by a variety of cell types and elicits its biological activity by interacting with specific G-protein coupled receptors found on platelets, neutrophils, and other inflammatory cells. The physiological consequences of the interaction of PAF with its receptor includes an increase in vascular permeability, hypotension, bronchoconstriction, and platelet and neutrophil aggregation. These biological effects are consistent with the concept that PAF is involved in a number of inflammatory diseases such as septic shock and asthma. Given the potent pathophysiological effects of PAF, a great deal of effort has been focused on the discovery of agents which block the action of PAF at its receptor. Within the past 10 years, a wide range of structures have been identified as PAF antagonists. These include not only PAF analogs, but also antagonists derived from natural products as well as non-lipid synthetic compounds. Several theories have been proposed to unify these diverse structural classes, but sophisticated molecular models of the receptor have not been widely employed. The discovery of new PAF antagonists has relied heavily on traditional medicinal chemistry approaches. A number of PAF antagonists have advanced to clinical evaluation. While several early compounds demonstrated efficacy in animal models of asthma they have failed to provide benefit for this condition in man. The current generation of potent antagonists are being evaluated as therapies for sepsis, pancreatitis and other disorders.

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15

Gomez, Federico P. y Robert Rodriguez-Roisin. "Platelet-Activating Factor Antagonists". BioDrugs 14, n.º 1 (julio de 2000): 21–30. http://dx.doi.org/10.2165/00063030-200014010-00003.

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16

Koltai, Matyas, David Hosford, Philippe Guinot, André Esanu y Pierre Braquet. "Platelet Activating Factor (PAF)". Drugs 42, n.º 1 (julio de 1991): 9–29. http://dx.doi.org/10.2165/00003495-199142010-00002.

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17

Koltai, Matyas y Pierre G. Braquet. "Platelet-activating factor antagonists". Clinical Reviews in Allergy 12, n.º 4 (diciembre de 1995): 361–80. http://dx.doi.org/10.1007/bf02802300.

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18

Saunders, R. N. y D. A. Handley. "Platelet-Activating Factor Antagonists". Annual Review of Pharmacology and Toxicology 27, n.º 1 (abril de 1987): 237–55. http://dx.doi.org/10.1146/annurev.pa.27.040187.001321.

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19

Chung, K. F. "Platelet activating factor revisited". Thorax 52, n.º 12 (1 de diciembre de 1997): 1019–20. http://dx.doi.org/10.1136/thx.52.12.1019.

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20

Roudebush, William. "Seminal Platelet-Activating Factor". Seminars in Thrombosis and Hemostasis 33, n.º 1 (febrero de 2007): 069–74. http://dx.doi.org/10.1055/s-2006-958464.

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21

Lee, Tae-Yoon. "Platelet Activating Factor-Acetylhydrolase". Yeungnam University Journal of Medicine 24, n.º 2 Suppl (31 de diciembre de 2007): S142–151. http://dx.doi.org/10.12701/yujm.2007.24.2s.s142.

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22

Honda, Z. i., S. Ishii y T. Shimizu. "Platelet-Activating Factor Receptor". Journal of Biochemistry 131, n.º 6 (1 de junio de 2002): 773–79. http://dx.doi.org/10.1093/oxfordjournals.jbchem.a003164.

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23

Stafforini, Diana M., Thomas M. McIntyre, Guy A. Zimmerman y Stephen M. Prescott. "Platelet-activating Factor Acetylhydrolases". Journal of Biological Chemistry 272, n.º 29 (18 de julio de 1997): 17895–98. http://dx.doi.org/10.1074/jbc.272.29.17895.

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24

Arai, Hiroyuki. "Platelet-activating factor acetylhydrolase". Prostaglandins & Other Lipid Mediators 68-69 (agosto de 2002): 83–94. http://dx.doi.org/10.1016/s0090-6980(02)00023-0.

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25

Ishii, Satoshi, Takahide Nagase y Takao Shimizu. "Platelet-activating factor receptor". Prostaglandins & Other Lipid Mediators 68-69 (agosto de 2002): 599–609. http://dx.doi.org/10.1016/s0090-6980(02)00058-8.

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26

Izumi, Takashi, Tomoko Takano, Haruhiko Bito, Motonao Nakamura, Hiroyuki Mutoh, Zen-ichiro Honda y Takao Shinizu. "Platelet-activating factor receptor". Journal of Lipid Mediators and Cell Signalling 12, n.º 2-3 (octubre de 1995): 429–42. http://dx.doi.org/10.1016/0929-7855(95)00028-o.

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27

Karpouza, Angeliki P. y Catherine Vakirtzi-Lemonias. "The platelet-activating factor acetylhydrolase of mouse platelets". Biochimica et Biophysica Acta (BBA) - Biomembranes 1323, n.º 1 (enero de 1997): 12–22. http://dx.doi.org/10.1016/s0005-2736(96)00178-2.

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28

Chesney, Carolyn M., D. David Pifer y Kim M. Huch. "Desensitization of human platelets by platelet activating factor". Biochemical and Biophysical Research Communications 127, n.º 1 (febrero de 1985): 24–30. http://dx.doi.org/10.1016/s0006-291x(85)80120-0.

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29

VALONE, F. "Synthesis of platelet-activating factor by human monocytes stimulated by platelet-activating factor". Journal of Allergy and Clinical Immunology 87, n.º 3 (marzo de 1991): 715–20. http://dx.doi.org/10.1016/0091-6749(91)90394-4.

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30

Bevers, Edouard, Theo Lindhout y Johan Heemskerk. "Platelet Activation and Blood Coagulation". Thrombosis and Haemostasis 88, n.º 08 (2002): 186–93. http://dx.doi.org/10.1055/s-0037-1613209.

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SummaryPlatelet activation and blood coagulation are complementary, mutually dependent processes in haemostasis and thrombosis. Platelets interact with several coagulation factors, while the coagulation product thrombin is a potent platelet-activating agonist. Activated platelets come in a procoagulant state after a prolonged elevation in cytosolic [Ca2+]i. Such platelets, e. g. when adhering to collagen via glycoprotein VI, expose phosphatidylserine (PS) at their outer surface and produce (PS-exposing) membrane blebs and microvesicles. Inhibition of aminophospholipid translocase and activation of phospholipid scramblase mediate the exposure of PS, whereas calpain-mediated protein cleavage leads to membrane blebbing and vesiculation. Surface-exposed PS strongly propagates the coagulation process by facilitating the assembly and activation of tenase and prothrombinase complexes. Factor IXa and platelet-bound factor Va support these activities. In addition, platelets can support the initiation phase of coagulation by providing binding sites for prothrombin and factor XI. They thereby take over the initiating role of tissue factor and factor VIIa in coagulation activation.

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31

SATOH, Kei, Shigeru TAKAMATSU, Yoko KAWAMURA, Seitoku MIZUNO, Bun-ichiro SHOJI y Mutsu TAKAMATSU. "Plasma Platelet-Activating Factor (PAF) Acetylhydrolase and Lipoproteins in Patients with Cerebral Thrombosis". Journal of Japan Atherosclerosis Society 15, n.º 3 (1987): 727–33. http://dx.doi.org/10.5551/jat1973.15.3_727.

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32

Schulam, P. G., A. Kuruvilla, G. Putcha, L. Mangus, J. Franklin-Johnson y W. T. Shearer. "Platelet-activating factor induces phospholipid turnover, calcium flux, arachidonic acid liberation, eicosanoid generation, and oncogene expression in a human B cell line." Journal of Immunology 146, n.º 5 (1 de marzo de 1991): 1642–48. http://dx.doi.org/10.4049/jimmunol.146.5.1642.

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Abstract Platelet-activating factor is a potent mediator of the inflammatory response. Studies of the actions of platelet-activating factor have centered mainly around neutrophils, monocytes, and platelets. In this report we begin to uncover the influence of platelet-activating factor on B lymphocytes. Employing the EBV-transformed human B cell line SKW6.4, we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine, phosphatidylinositol, and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M. The inactive precursor, lyso-platelet-activating factor, at a concentration as high as 10(-7) M had no effect on any of the membrane phospholipids. We also show that platelet-activating factor from 10(-12) to 10(-6) M induced rapid and significant elevation in intracellular calcium levels, whereas lyso-platelet-activating factor was again ineffective. We further demonstrate the impact of platelet-activating factor binding to B cells by measuring platelet-activating factor induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production. Moreover, platelet-activating factor was capable of inducing transcription of the nuclear proto-oncogenes c-fos and c-jun. Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous 5-lipoxygenase activity modulates platelet-activating factor induced arachidonic acid release perhaps acting at the level of phospholipase A2. In summary, platelet-activating factor is shown here to have a direct and profound effect on a pure B cell line.

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33

Duronio, Vincent, Anne Reany, Sandra Wong, Chantal Bigras y Hassan Salari. "Characterization of platelet-activating factor receptors in porcine platelets". Canadian Journal of Physiology and Pharmacology 68, n.º 12 (1 de diciembre de 1990): 1514–19. http://dx.doi.org/10.1139/y90-230.

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Despite a large number of studies describing the properties and effects of platelet-activating factor (PAF), little is known about its receptor structure. The characterization of the PAF receptor from additional cell types and species is important for the design of strategies to purify and characterize the receptor molecule. Porcine platelets were shown to bind PAF with characteristics similar to several other species, based on receptor number, affinity, and the activity of PAF antagonists. We found that the affinity for binding was higher in porcine than in rabbit platelets (Kd = 0.68 ± 0.13 nM for rabbit and 0.29 ± 0.10 nM for porcine). Porcine platelets have approximately 281 ± 158 receptors per cell compared with 689 ± 229 receptors in rabbit platelets. Rabbit platelets respond to concentrations of PAF that are approximately 105-fold lower than those required for aggregation of porcine platelets, but this difference is probably not due to the differences in receptor number alone. When binding was compared between purified membranes from these two cell types, porcine platelets had 20-fold fewer receptors per milligram of membrane protein, but this difference may have been due to an artifact of the membrane preparation procedure. Binding of PAF was severely hindered at cold temperatures. It was undetectable in whole cells on ice and greatly reduced with purified membranes. This study is the first to characterize PAF receptors in porcine platelets, which represent a potentially useful source of receptor for further biochemical characterization.Key words: platelet activating factor, receptor, porcine, platelet, membrane.

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34

Potron, G., E. Petitfrere y P. Nguyen. "Platelet activating factor and ischemia". Clinical Hemorheology and Microcirculation 13, n.º 2 (1993): 155–76. http://dx.doi.org/10.3233/ch-1993-13202.

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35

O'Neill, C. "Embryo-derived platelet activating factor". Reproduction, Fertility and Development 4, n.º 3 (1992): 283. http://dx.doi.org/10.1071/rd9920283.

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Platelet-activating factor (PAF) is secreted by the preimplantation embryo of a number of species. The role of this secretion is yet to be fully elucidated. Evidence to date indicates that it has an important function as an autocrine stimulant of embryonic metabolism, growth and viability. Production of PAF by embryos appears to be severely compromised in vitro. This may be a major cause of reduced embryo viability following embryo culture and it may also help to explain the controversy in the literature regarding the production of PAF by embryos. PAF also alters several aspects of maternal physiology during early pregnancy including endometrial prostaglandin secretion. The significance of these changes remains to be defined.

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36

Greaves, M. W. y M. R. Judge. "Platelet activating factor in psoriasis". British Journal of Dermatology 136, n.º 3 (marzo de 1997): 467. http://dx.doi.org/10.1111/j.1365-2133.1997.tb14968.x.

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37

O'NEILL, CHRISTOPHER, MELANIE COLLIER y DOUGLAS M. SAUNDERS. "Embryo-Derived Platelet-Activating Factor." Annals of the New York Academy of Sciences 541, n.º 1 In Vitro Fert (octubre de 1988): 398–406. http://dx.doi.org/10.1111/j.1749-6632.1988.tb22276.x.

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38

Tsuda, Makoto, Hidetoshi Tozaki-Saitoh y Kazuhide Inoue. "Platelet-Activating Factor and Pain". Biological & Pharmaceutical Bulletin 34, n.º 8 (2011): 1159–62. http://dx.doi.org/10.1248/bpb.34.1159.

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39

Pałgan, Krzysztof y Zbigniew Bartuzi. "Platelet activating factor in allergies". International Journal of Immunopathology and Pharmacology 28, n.º 4 (20 de octubre de 2015): 584–89. http://dx.doi.org/10.1177/0394632015600598.

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40

Minhas, B. S., B. A. Ripps, Y. P. Zhu, H. N. Kim, T. H. Burwinkel y N. Gleicher. "Platelet Activating Factor and Conception". American Journal of Reproductive Immunology 35, n.º 3 (marzo de 1996): 267–71. http://dx.doi.org/10.1111/j.1600-0897.1996.tb00043.x.

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41

Stafforini, Diana M., Stephen M. Prescott, Guy A. Zimmerman y Thomas M. McIntyre. "Mammalian platelet-activating factor acetylhydrolases". Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1301, n.º 3 (junio de 1996): 161–73. http://dx.doi.org/10.1016/0005-2760(96)00040-9.

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42

Barnes, Peter J. "Platelet-activating factor and asthma". Journal of Allergy and Clinical Immunology 81, n.º 1 (enero de 1988): 152–60. http://dx.doi.org/10.1016/0091-6749(88)90234-5.

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43

Peters, Ulrike, Wassja Bankova y Peter Welzel. "Platelet activating factor synthetic studies". Tetrahedron 43, n.º 16 (enero de 1987): 3803–16. http://dx.doi.org/10.1016/s0040-4020(01)86866-6.

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44

BARNES, PETER J. "Platelet Activating Factor and Asthma". Annals of the New York Academy of Sciences 629, n.º 1 Advances in t (julio de 1991): 193–204. http://dx.doi.org/10.1111/j.1749-6632.1991.tb37976.x.

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45

Morley, J. "Platelet activating factor and asthma". Agents and Actions 19, n.º 1-2 (octubre de 1986): 100–108. http://dx.doi.org/10.1007/bf01977264.

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46

Karasawa, Ken, Noriko Satoh, Toshio Hongo, Yasuhito Nakagawa, Morio Setaka y Shoshichi Nojima. "Radioimmunoassay for platelet-activating factor". Lipids 26, n.º 12 (diciembre de 1991): 1126–29. http://dx.doi.org/10.1007/bf02536515.

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47

Furukawa, Masayuki, Edward L. Lee y John M. Johnston. "Platelet-Activating Factor–Induced Ischemic Bowel Necrosis: The Effect of Platelet-Activating Factor Acetylhydrolase". Pediatric Research 34, n.º 2 (agosto de 1993): 237–41. http://dx.doi.org/10.1203/00006450-199308000-00027.

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48

Masugi, Fuminori, Toshio Ogihara, Shuichi Saeki, Katsuhiko Sakaguchi, Yuichi Kumahara, Kiyoshi Satouchi, Makoto Oda, Kunihiko Saito y Koh Tokunaga. "Endogenous platelet-activating factor and anti-platelet-activating factor in patients with renovascular hypertension". Life Sciences 42, n.º 4 (enero de 1988): 455–60. http://dx.doi.org/10.1016/0024-3205(88)90084-7.

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49

Travers, Jeffrey B., Qian Li, Howard Sprecher y Richard H. Fertel. "Binding of carbamyl-platelet-activating factor to the raji lymphoblast platelet-activating factor receptor". International Journal of Immunopharmacology 14, n.º 4 (mayo de 1992): 515–23. http://dx.doi.org/10.1016/0192-0561(92)90112-x.

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50

Mabuchi-Itoh, Kiyoko, Takayuki Sugiura, Neng-neng Cheng y Keizo Waku. "Aspirin induces non-enzymatic formation of platelet-activating factor from lyso platelet-activating factor". FEBS Letters 332, n.º 3 (18 de octubre de 1993): 233–36. http://dx.doi.org/10.1016/0014-5793(93)80639-c.

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