FOLLOWUS
1. College of Health Information Technology and Management, Shanghai University of Medicine and Health Sciences,Shanghai,China
2. Department of Cardiologic Medicine, The Second People’s Hospital of Fujian Province,Fuzhou,China
3. The Second Clinic of Chinese Medicine, Fujian University of Traditional Chinese Medicine,Fuzhou,China
纸质出版日期:2017,
网络出版日期:2017-2-15,
Scan for full text
Zheng, Gh., Xiong, Sq., Chen, Hy. et al. Association of platelet-activating factor receptor gene rs5938 (G/T) and rs313152 (T/C) polymorphisms with coronary heart disease and blood stasis syndrome in a Chinese Han population., Chin. J. Integr. Med. 23, 893–900 (2017). https://doi.org/10.1007/s11655-017-2802-4
Guo-hua Zheng, Shang-quan Xiong, Hai-ying Chen, et al. Association of platelet-activating factor receptor gene rs5938 (G/T) and rs313152 (T/C) polymorphisms with coronary heart disease and blood stasis syndrome in a Chinese Han population[J]. Chinese Journal of Integrative Medicine, 2017,23(12):893-900.
Zheng, Gh., Xiong, Sq., Chen, Hy. et al. Association of platelet-activating factor receptor gene rs5938 (G/T) and rs313152 (T/C) polymorphisms with coronary heart disease and blood stasis syndrome in a Chinese Han population., Chin. J. Integr. Med. 23, 893–900 (2017). https://doi.org/10.1007/s11655-017-2802-4 DOI:
Guo-hua Zheng, Shang-quan Xiong, Hai-ying Chen, et al. Association of platelet-activating factor receptor gene rs5938 (G/T) and rs313152 (T/C) polymorphisms with coronary heart disease and blood stasis syndrome in a Chinese Han population[J]. Chinese Journal of Integrative Medicine, 2017,23(12):893-900. DOI: 10.1007/s11655-017-2802-4.
To explore the association of the platelet-activating factor receptor (PAFR) gene rs5938
rs313152 and rs76744145 polymorphisms with coronary heart disease (CHD) and blood stasis syndrome (BSS) of CHD in Chinese Han population. A total of 570 CHD patients (299 with BSS and 271 with non-BSS) and 317 controls were enrolled. The PAFR gene rs5938
rs313152 and rs76744145 polymorphisms were genotyped using the multiplex SNaPshot technology. The statistical analysis was conducted using a multiple variable logistic regression model. Significant differences were detected in the genotypes frequency distributions of the rs5938 (P<0.01)
but not the rs313152 (P>0.05)
between the controls and CHD patients. Individuals with an rs5938 or rs313152 mutated allele had a low risk for CHD [adjusted odds ratio (aOR)=0.35
95% confidence interval (CI): 0.23 to 0.56
P<0.01; aOR=0.65
95% CI: 0.46 to 0.91
P<0.05
respectively]. After the CHD patients were stratified as BSS or non-BSS according to their Chinese medicine patterns
the rs5938 polymorphism mutated alleles had a significant association with a low risk for BSS of CHD (aOR=0.32
95% CI: 0.18 to 0.57
P<0.01) and non-BSS of CHD (aOR=0.31
95% CI: 0.17 to 0.55
P<0.01). The rs313152 polymorphism was associated with a low risk for BSS (aOR=0.51
95% CI: 0.33 to 0.79
P<0.01)
but not for non-BSS (aOR=1.22
95% CI: 0.81 to 1.85
P<0.05). Furthermore
the interaction effect of the rs5938 and rs313152 polymorphisms for BSS of CHD was significantly based on an aOR value associated with the combination of the rs5938 GT genotype with the rs313152 TC genotype of 0.27 (95% CI: 0.1 to 0.7
P<0.01). The PAFR gene rs5938 or rs313152 polymorphisms might be a potential biomarker for susceptibility to CHD
especially to BSS of CHD in Chinese Han population.
To explore the association of the platelet-activating factor receptor (PAFR) gene rs5938
rs313152 and rs76744145 polymorphisms with coronary heart disease (CHD) and blood stasis syndrome (BSS) of CHD in Chinese Han population. A total of 570 CHD patients (299 with BSS and 271 with non-BSS) and 317 controls were enrolled. The PAFR gene rs5938
rs313152 and rs76744145 polymorphisms were genotyped using the multiplex SNaPshot technology. The statistical analysis was conducted using a multiple variable logistic regression model. Significant differences were detected in the genotypes frequency distributions of the rs5938 (P<0.01)
but not the rs313152 (P>0.05)
between the controls and CHD patients. Individuals with an rs5938 or rs313152 mutated allele had a low risk for CHD [adjusted odds ratio (aOR)=0.35
95% confidence interval (CI): 0.23 to 0.56
P<0.01; aOR=0.65
95% CI: 0.46 to 0.91
P<0.05
respectively]. After the CHD patients were stratified as BSS or non-BSS according to their Chinese medicine patterns
the rs5938 polymorphism mutated alleles had a significant association with a low risk for BSS of CHD (aOR=0.32
95% CI: 0.18 to 0.57
P<0.01) and non-BSS of CHD (aOR=0.31
95% CI: 0.17 to 0.55
P<0.01). The rs313152 polymorphism was associated with a low risk for BSS (aOR=0.51
95% CI: 0.33 to 0.79
P<0.01)
but not for non-BSS (aOR=1.22
95% CI: 0.81 to 1.85
P<0.05). Furthermore
the interaction effect of the rs5938 and rs313152 polymorphisms for BSS of CHD was significantly based on an aOR value associated with the combination of the rs5938 GT genotype with the rs313152 TC genotype of 0.27 (95% CI: 0.1 to 0.7
P<0.01). The PAFR gene rs5938 or rs313152 polymorphisms might be a potential biomarker for susceptibility to CHD
especially to BSS of CHD in Chinese Han population.
platelet-activating factor receptorgene polymorphismcoronary heart diseaseBlood Stasis SyndromesusceptibilityChinese Medicine
platelet-activating factor receptorgene polymorphismcoronary heart diseaseBlood Stasis SyndromesusceptibilityChinese Medicine
Ross R. Atherosclerosis—an inflammatory disease. N Engl J Med 1999;340:115–126.
Ross R. The pathogenesis of atherosclerosis: a perspective for the 90s. Nature 1993;362:801–809.
Stafforini DM, McIntyre TM, Zimmerman GA, Prescott SM. Platelet-activating factor, a pleiotrophic mediator of physiological and pathological processes. Crit Rev Clin Lab Sci 2003;40:643–672.
Demopoulos CA, Karantonis HC, Antonopoulou S. Platelet activating factor—a molecular link between atherosclerosis theories. Eur J Lipid Sci Tech 2003;105:705–716.
Welch EJ, Nalkawadi RP, Li Z, Lin P, Ishii S, Shimizu T, et al. Opposing effects of platelet-activating factor and lyso-platelet activating factor on neutrophil and platelet activation. Mol Pharmacol 2009;75:227–234.
Uhlig S, Goggel R, Engel S. Mechanisms of plateletactivating factor (PAF)-mediated responses in the lung. Pharmacol Rep 2005;57(Suppl):206–221.
Arakawa H, Qian JY, Baatar D, Karasawa K, Asada Y, Sasaguri Y, et al. Local expression of platelet-activating factoracetylhydrolase reduces accumulation of oxidized lipoproteins and inhibits inflammation, shear stress-induced thrombosis, and neointima formation in balloon-injured carotid arteries in nonhyperlipidemic rabbits. Circulation 2005;111:3302–3309.
Pégorier S, Stengel D, Durand H, Croset M, Ninio E. Oxidized phospholipid: POVPC binds to platelet-activatingfactor receptor on human macrophages. Implications in atherosclerosis. Atherosclerosis 2006;188:433–443.
Grigg J. The platelet activating factor receptor: a new antiinfective target in respiratory disease? Thorax 2012;67:840–841.
Marrache AM, Gobeil F Jr, Bernier SG, Stankova J, Rola- Pleszczynski M, Choufani S, et al. Proinflammatory gene induction by platelet-activating factor mediated via its cognate nuclear receptor. J Immunol 2002;169:6474–6481.
Stafforini DM, McIntyre TM, Zimmerman GA, Prescott SM. Platelet-activating factor, a pleiotrophic mediator of physiological and pathological processes. Crit Rev Clin Lab Sci 2003;40:643–672.
Bazan NG. Synaptic lipid signaling: significance of polyunsaturated fatty acids and platelet-activating factor. J Lipid Res 2003;44:2221–2233.
Iovino F, Brouwer MC, van de Beek D, Molema G, Bijlsma JJ. Signalling or binding: the role of the platelet-activating factor receptor in invasive pneumococcal disease. Cell Microbiol 2013;15:870–881.
Wu LQ, Ouyang XY, Liu Y, Peng SY, Wang L, Wang WJ. Inhibitory effects of SY0916, a platelet-activating factor receptor antagonist, on the angiogenesis of human umbilical vascular endothelial cells. J Asian Nat Prod Res 2011;13:984–992.
Pei Y, Dy LC, Natarajan S, Travers JB. Activation of the epidermal platelet-activating factor receptor result in ICAM-1 expression. In Vitro Cell Dev Biol Anim 2000;36:11–13.
Andréasson E, Önnheim K, Forsman H. The subcellular localization of the receptor for platelet-activating factor in neutrophils affects signaling and activation characteristics. Clin Dev Immunol 2013;2013:456–407.
Papadopoulou C, Corrigall V, Taylor PR, Poston RN. The role of the chemokines MCP-1, GRO-α, IL-8 and their receptors in the adhesion of monocytic cells to human atherosclerotic plaques. Cytokine 2008;43:181–186.
Rohatgi A, Owens AW, Khera A, Ayers CR, Banks K, Das SR, et al. Differential associated between soluble cellular adhesion molecules and atherosclerosis in the dallas heart study: a distnct role for soluble endothelial cell-selective adhesion molecule. Arterioscler Thromb Vasc Biol 2009;29:1684–1690.
Fukunaga K, Ishii S, Asano K, Yokomizo T, Shiomi T, Shimizu T, et al. Single nucleotide polymorphism of human platelet-activating factor receptor impairs G-protein activation. J Biol Chem 2001;276:43025–43030.
Brzustowicz LM, Gardner JP, Hopp L, Jeanclos E, Ott J, Yang XY, et al. Linkage analysis using platelet-activating factor Ca2+ response in transformed lymphoblasts. Hypertension 1997;29:158–164.
Ishii S, Shimizu T. Platelet-activating factor (PAF) receptor and genetically engineered PAF receptor mutant mice. Prog Lipid Res 2000;39:41–82.
Osoegawa M, Miyagishi R, Ochi H, Nakamura I, Niino M, Kikuchi S, et al. Platelet-activating factor receptor gene polymorphism in Japanese patients with multiple sclerosis. J Neuroimmunol 2005;161:195–198.
Messadi A, Fekih-Mrissa N, Zaouali J, Layouni S, Nsiri B, Yedeas M, et al. Implication of platelet-activating factor receptor A224D mutation in susceptibility to relapsingremitting multiple sclerosis: a Tunisian population study. Pathol Biol (Paris) 2012;60:185–189.
Nagase T, Ishii S, Kume K, Uozumi N, Izumi T, Ouchi Y, et al. Platelet-activating factor mediates acid-induced lung injury in genetically engineered mice. J Clin Invest 1999;104:1071–1076.
Ninio E, Tregouet D, Carrier JL, Stengel D, Bickel C, Perret C, et al. Platelet-activating factor-acetylhydrolase and PAF-receptor gene haploytpes in relation to future cardiovascular events in patients with coronary artery disease. Human Molecular Genetics 2004;13:1341–1351.
Su SB, Lu AP, Li S, Jia W. Evidence-based ZHENG: a traditional Chinese medicine syndrome. Evid Based Complement Alternat Med 2012;2012.
Ren Y, Zhang MZ, Chen KJ, You S, Li J, Guo L, et al. Clinical and epidemiological investigation of CM syndrome of patients with coronary heart disease in China. Evid Based Complement Alternat Med 2012;2012:714517.
Chen KJ, Xue M, Yin H. The relationship between platelet activation and coronary heart disease and blood-stasis syndrome. J Capit Med Univ 2008;29:266–269.
European Society of Cardiology, American College of Cardiology. Myocardial infarction redefined—a consensus document of the joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction. Eur Heart J 2000;21:1502–1513.
Writing group on behalf of the participating experts of the WHO consultation for revision of WHO definition of myocardial infarction. World Health Organization definition of myocardial infarction: 2008-09 revision. Int J Epidemiol 2011;40:139–146.
Disease Special Committee, Chinese Association of the Integrative Medicine. Standard of syndrome differentiation on coronary heart disease of Chinese medicine. Chin J Integr Tradit West Med (Chin) 1991;11:257.
Shi ZX, Gu WL. Exploration of CM syndrome differentiation of coronary heart disease and coronary arteriography. Chin J Integr Tradit West Med (Chin) 2007;27:76–79.
Li SM, Xu H, Chen KJ. The diagnostic criteria of bloodstasis syndrome: considerations for standardization of pattern identification. Chin J Integr Med 2014;20:483–489.
Anthony D, George P, Eaton CB. Cardiac risk factors: environmental, sociodemographic, and behavioral cardiovascular risk factors. FP Essent 2014;421:16–20.
Roifman I, Beck PL, Anderson TJ, Eisenberg MJ, Genest J. Chronic inflammatory diseases and cardiovascular risk: a systematic review. Can J Cardiol 2011 27:174–182.
Langer HF, Bigalke B, Seizer P, Stellos K, Fateh-Moghadam S, Gawaz M. Interaction of platelets and inflammatory endothelium in the development and progression of coronary artery diseases. Semin Thromb Hemost 2010,36:131–138.
Montrucchio G, Alloatti G, Camussi G. Role of plateletactivating factor in cardiovascular pathophysiology. Physiol Rev 2000;80:1669–1699.
Gilli UO, Schneider MK, Loetscher P, Seebach JD. Human polymorphonuclear neutrophils are recruited by porcine chemokines acting on CXC chemokine receptor 2, and platelet-activating factor. Transplantation 2005;79:1324–1331.
Welch EJ, Nalkawadi RP, Li Z, Lin P, Ishii S, Shimizu T, et al. Opposing effects of platelet-activating factor and lyso-platelet activating factor on neutrophil and platelet activation. Mol Pharmacol 2009;75:227–234.
Michalis LK, Tambaki AP, Katsouras CS, Goudevenos JA, Kolettis T, Adamides K, et al. Platelet hyperaggregability to platelet activating factor (PAF) in non-ST elevation acute coronary syndromes. Curr Med Res Opin 2002;18:108–112.
Garcia CC, Russo RC, Guabiraba R, Fagundes CT, Polidoro RB, Tavares LP, et al. Platelet-activating factor receptor plays a role in lung unjury and death caused by influenza A in mice. PloS Pathog 2010; 6:e1001171.
Guerrero AT, Zaperlon AC, Vieira SM, Pinto LG, Ferreira SH, Cunha FQ, et al. The role of PAF/PAFR signaling in zymosan-induced articular inflammatory hyperalgesia. Naunyn Schmiedebergs Arch Pharmacol 2013;386:51–59.
Moharam BA, Jantan l, Jalil J, Shaari K. Inhibitory effects of phylligenin and quebrachitol isolated form mitrephora vulpine on platelet activating factor receptor binding and platelet aggregation. Molecules 2010;15:7840–7848.
Chao W, Olson MS. Platelet-activatng factor: receptor and signal transduction. Biochem J 1993;292:617–629.
Fang Y, Xu H, Qu D, Zheng F, Shi DZ, Chen KJ. Study on the tongue manifestations for the blood stasis and toxin syndrome in the stable patients of coronary heart disease. Chin J Integr Med 2011;17:333–338.
Ishioka H, Sonoda A, Asano K, Fukunaga K, Yamaguchi K, Takeshita E, et al. A polymorphism in a cytoplasmic domain of platelet-activating factor receptor (PAF-R), (224) Ala/Asp, affects PAF-induced signaling and may cause inter-individual variation of platelet responsiveness to PAF. Blood 2001;98:242A.
Xue M, Chen KJ, Yin HJ. Relationship between platelet activation related factors and polymorphism of related gene in patients with coronary heart disease of blood stasis syndrome. Chin J Integr Med 2008;14:267–273.
0
浏览量
0
Downloads
1
CSCD
关联资源
相关文章
相关作者
相关机构