期刊文献+

冠心病患者血小板CD31及血浆纤维蛋白原表达水平的测定及其意义 被引量:1

Expression level and clinical significance of platelet CD31 and plasma fibrinogen in patients with coronary heart disease
下载PDF
导出
摘要 目的检测冠心病(CHD)患者血小板内皮细胞黏附分子1(CD31)及血浆纤维蛋白原(FIB)水平,分析其与CHD严重程度的相关性并探讨其临床意义。方法入选研究对象97例,分为稳定型心绞痛(SAP)组(21例),急性冠脉综合征(ACS)组(43例)和正常对照组(33例)。采用流式细胞术检测血小板CD31,凝固法测定血浆FIB的表达水平。结果 ACS组血小板表面活性标志物CD31[(93.85±14.84)%],血浆FIB水平[(3.66±0.91)g/L]均明显高于对照组[(78.69±27.09)%,(3.06±0.62)g/L]和SAP组[(82.80±28.00)%,(3.14±0.56)g/L(均为P<0.05)];而对照组与SAP组CD31、FIB表达水平差异无统计学意义(均为P>0.05)。相关分析显示CD31与FIB呈显著正相关(r=0.337,P<0.01)。结论检测CHD患者CD31、FIB水平,能较好地反映CHD严重程度,对临床有重要的应用价值。 Objective To study the expression level and clinical significance of platelet endothelial cells adhesion molecule-1(CD31) and plasma fibrinogen(FIB) in patients with coronary heart disease(CHD). Methods A total of 97 patients,including 21 patients with stable angina pectoris(SAP group),43 with acute coronary syndrome(ACS group) and 33 controls(control group)were studied.The expression level of platelet CD31 was measured by flow cytometry and plasma FIB was measured by coagulation method. Results The expression level of platelet CD31 [(93.85±14.84)%] and plasma FIB [(3.66±0.91)g/L] in ACS group were significantly higher than in control group [(78.69 ±27.09)% and(3.06±0.62)g/L)] and SAP group [(82.80±28.00)% and(3.14±0.56)g/L](all P0.05).There were no significant differences in platelet CD31 and plasma FIB between control group and SAP group(P0.05).Correlation analysis demonstrated that platelet CD31 was positively correlated with plasma FIB(r=0.337,P0.01). Conclusions The expression level of platelet CD31 and plasma FIB in CHD patients can reflect the severity of disease and has important clinical values.
出处 《中国心血管杂志》 2012年第5期354-356,共3页 Chinese Journal of Cardiovascular Medicine
基金 大连市科技局科技计划项目(2008J22JH016)~~
关键词 冠心病 血小板内皮细胞黏附分子1 纤维蛋白原 Coronary heart disease CD31/PECAM-1 Fibrinogen
  • 相关文献

参考文献10

  • 1Goldschmidt Clermont PJ, Creager MA, Losordo DW, et al. Atherosclerosis 2005: recent discoveries and novel hypotheses. Circulation, 2005, 112: 3348-3353.
  • 2陆再英,钟南山主编.内科学.第七版.北京:人民卫生出版社,2008.131-133.
  • 3Thygesen K, Alpert JS, White HD. Joint ESC/ACCF/AHA/ WHF task force for the redefinition of myocardial iffarction. Universal definition of myocardial infarction. J Am Coil Cardiol, 2007, 50: 2173-2195.
  • 4Patil S, Newman DK, Newman PJ. Platelet endothelial cell adhesion molecule-1 serves as an inhibitory receptor that modulates platelet responses to collagen. Blood, 2001, 97: 1727-1732.
  • 5Soeki T, Tamura Y, Shinohara H, et al. Increased soluble platelet/endothelial cell adhesion molecule-1 in the early stages of acute coronary syndromes. Int J Cardiol, 2003, 90: 261-268.
  • 6del Zoppo G J, Levy DE, Wasiewski WW, et aL Hyperfibrinogenemia and functional outcome from acute ischemic stroke. Stroke, 2009, d0: 1687-1691.
  • 7del Zoppo G J, Levy DE, Wasiewski WW, et al. Hyperfibrinogenemia and functional outcome from acute ischemic stroke. Stroke, 2009, 40: 1687-1691.
  • 8赵韶华,高海青,邱洁.前纤维蛋白-1对内皮功能影响的研究进展[J].中华老年医学杂志,2011,30(9):784-787. 被引量:14
  • 9Nourshargh S,Krombach F, Dejana E. The role of JAM-A and PECtkM-I in modulating leukocyte infiltration in ifflamed and ischemic tissues. J Leukoc Biol, 2006, 80: 714-718.
  • 10Dangerfield J,Larbi KY, Huang MT, et al. PECAM-1 (CD31) homophilic interaction up-regulates alpha6betal on transmigrated neutrophils in vivo and plays a functional role in the ability of alpha6 integrins to mediate leukocyte migration through the perivascular basement membrane. J Exp Med, 2002, 196 : 1201- 1211.

二级参考文献34

  • 1Ding Z, Lambrechts A,Parepally M, et al. Silencing Profilin-1 inhibits endothelial cell proliferation, migration and cord morphogenesis. J Cell Sci, 2006, 119 :4127-4137.
  • 2Evans NJ, Walker JW. Endothelin-1 mobilizes pfnl- bound PIP2 in cardiac. Muscle Exp Biol Med, 2006, 231:882-887.
  • 3Bayoumi M,Alhaj MA, E1-Sayed O, et al. Vascular hypertrophy and hypertension caused by transgenic overexpression of profilin 1. J Biol Chem, 2007, 52 37632-37639.
  • 4Behnen M, Murk K, Kursula P, et al . Testis- expressed profilins 3 and 4 show distinct functional characteristics and localize in the acroplaxome- manchette complex in spermatids. BMC Cell Biol, 2009, 10 : 34-50.
  • 5Bulinski JC. Cell biology. G-actin discrimination. Science, 2006, 313:180-181.
  • 6Witke W. The role of profilin complexes in cell motility and other cellular processes. Trends Cell Biol,2004, 14: 461-469.
  • 7Pollard TD, Borisy GG. Cellular motility driven by assembly and disassembly of G-actin filaments. Cell, 2003, 112: 453-465.
  • 8Birbach, R. Profilin, a multi-modal regulator of neuronal plasticity. Bio Essays,2008, 30: 994-1002.
  • 9Suetsugu S, Miki H, Takenawa T. The essential role of profilin in the assembly of G-actin for microspike formation. EmboJ, 1998,17: 6516-6526.
  • 10Carlsson L, Nystrom LE,Sundkvist I, et al. G-actin polymerizability is influenced by profilin, a low molecular weight protein in nonmuscle cells. J Moi Biol, 1977,115: 465-483.

共引文献28

同被引文献4

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部