脑梗死患者血小板膜糖蛋白Ⅰ bα基因HPA-2、Kozak位点多态性分析  

Polymorphism and significance of platelet membrane glycoprotein Ⅰbα gene HPA-2,Kozak sites in patients with cerebral infarction

作　　者：张爱琴[1] 郑敏[1] 郝跃伟[1] 赵婷婷[1] 刘雪平[1] 

机构地区：[1]山东大学附属省立医院,济南250021

出　　处：《山东医药》2010年第38期23-24,共2页Shandong Medical Journal

基　　金：山东省科学技术发展计划资助项目(2002BB1DBA6)

摘　　要：目的观察脑梗死患者血小板膜糖蛋白(GP)Ⅰbα基因HPA-2、Kozak位点多态性,探讨其与脑梗死的关系。方法选取316例经CT或MR I证实的脑梗塞患者(观察组)及209例无脑血管疾病者(对照组),采用聚合酶链反应—限制性片断长度多态性(PCR-RFLP)法检测GPⅠbα基因HPA-2、Kozak位点多态性,用流式细胞术(FCM)测定血小板活化标志物CD62P、CD63的表达。结果观察组血小板GPⅠbα基因HPA-2位点基因型分布及等位基因频率与对照组相比P均>0.05;观察组Kozak位点观察组基因型为CC者20例、CT者113例、TT者169例,等位基因C频率为25.33%、T频率为74.67%;对照组分别为6、28、162例和10.20%、89.80%。两组基因型分布和等位基因C、T频率相比,P均<0.05。观察组表达等位基因C者(基因型CC+CT)CD62P表达量为20.94±7.35、CD63表达量为28.62±9.47,不表达等位基因C者(基因型为TT)分别为13.36±6.27、20.27±5.45,二者CD62P、CD63表达量相比P均<0.05。结论 脑梗死患者血小板GPⅠbα基因Kozak位点存在多态性,HPA-2位点未发现多态性。GPⅠbα基因Kozak位点多态性可能通过影响血小板的活化参与脑梗死的发生过程。Objective To observe the polymorphism of platelet membrane glycoprotein Ⅰbα gene HPA-2,Kozak sites in patients with cerebral infarction,and explore its significance.Methods The expression of platelet glycoprotein（CD62P,CD63）was measured by flowing cytometry（FCM） in 316 patients with cerebral infarction and 209 control subjects.GpⅠbαgenotype was investigated by RT-PCR.Results The expression of platelet glycoprotein CD62p,CD63 in cerebral infarction patients were significantly higher than that of the controls.There were no significant differences in GpⅠbα HPA-2 genotype frequencies and allele frequencies between cerebra vascular thrombosis patients and controls.Kozak genotypes with C allele were 25.95% in CVD group,compared with that of control group（18.18%）.Statistics signs showed significant differences（P=0.0033）.Conclusions There is platelet membrane glycoprotein Ⅰbα gene HPA-2,Kozak sites polymorphism in patients with cerebral infarction.It may participate the generate of cerebral infraction by affect platelet activation.

关 键 词：血小板糖蛋白 基因多态性 缺血性脑卒中 脑梗死 

分 类 号：R742[医药卫生—神经病学与精神病学]