中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2009年
6期
509-513
,共5页
谭晓秋%杨艳%刘智飞%白志茹%周文%裴杰%陈桂兰%曾晓荣
譚曉鞦%楊豔%劉智飛%白誌茹%週文%裴傑%陳桂蘭%曾曉榮
담효추%양염%류지비%백지여%주문%배걸%진계란%증효영
心房颤动%钾通道%基因表达
心房顫動%鉀通道%基因錶達
심방전동%갑통도%기인표체
Atrial fibrillation%Potassium channels%Gene expression
目的 心房颤动(房颤)是最为常见的快速性心律失常之一.钾通道相关蛋白2(K+channel interacting protein 2,KChIP2)是心肌细胞瞬时外向钾通道的重要辅助亚单位,在,Ito发挥正常功能中起着重要的作用.报告采用实时荧光定量聚合酶链反应(PCR)技术通过对房颤时KChIP2和Kv4.3基因mRNA水平进行定量研究,探讨KChIP2在房颤中的作用和对于瞬时外向钾通道的可能调控机制.方法 (1)30例风湿性心脏病患者分为两组:窦性心律组(窦律组)13例,持续性房颤组(房颤组)17例,取其常规切除的右心耳组织作为研究对象;(2)提取心房肌组织总RNA,通过RT-PCR和TA克隆技术构建含有目的 基因片段的质粒标准品;(3)以GAPDH为内参照基因,采用SYBR Green I法实时荧光定量PCR技术检测持续性房颤和窦律患者KChIP2和Kv4.3基因mRNA水平.结果 (1)标准曲线和熔解曲线:标准曲线线性关系良好,相关系数R2＞0.99.熔解曲线呈明显单峰状,退火温度与预测值基本一致;(2)窦律组和房颤组KChIP2/GAPDH比值分别为0.2200±0.0388、0.1468±0.0452,房颤组KChIP2基因mRNA水平低于窦律组,P＜0.01;窦律组和房颤组Kv4.3/GAPDH比值分别为0.5257±0.1427、0.3946±0.1826,房颤组Kv4.3基因mRNA水平低于窦律组,P＜0.05.结论 与窦律患者相比,房颤患者KChIP2基因和Kv4.3基因明显下调,KChIP2和Kv4.3基因下调是房颤时Ito电流下调的分子基础.
目的 心房顫動(房顫)是最為常見的快速性心律失常之一.鉀通道相關蛋白2(K+channel interacting protein 2,KChIP2)是心肌細胞瞬時外嚮鉀通道的重要輔助亞單位,在,Ito髮揮正常功能中起著重要的作用.報告採用實時熒光定量聚閤酶鏈反應(PCR)技術通過對房顫時KChIP2和Kv4.3基因mRNA水平進行定量研究,探討KChIP2在房顫中的作用和對于瞬時外嚮鉀通道的可能調控機製.方法 (1)30例風濕性心髒病患者分為兩組:竇性心律組(竇律組)13例,持續性房顫組(房顫組)17例,取其常規切除的右心耳組織作為研究對象;(2)提取心房肌組織總RNA,通過RT-PCR和TA剋隆技術構建含有目的 基因片段的質粒標準品;(3)以GAPDH為內參照基因,採用SYBR Green I法實時熒光定量PCR技術檢測持續性房顫和竇律患者KChIP2和Kv4.3基因mRNA水平.結果 (1)標準麯線和鎔解麯線:標準麯線線性關繫良好,相關繫數R2＞0.99.鎔解麯線呈明顯單峰狀,退火溫度與預測值基本一緻;(2)竇律組和房顫組KChIP2/GAPDH比值分彆為0.2200±0.0388、0.1468±0.0452,房顫組KChIP2基因mRNA水平低于竇律組,P＜0.01;竇律組和房顫組Kv4.3/GAPDH比值分彆為0.5257±0.1427、0.3946±0.1826,房顫組Kv4.3基因mRNA水平低于竇律組,P＜0.05.結論 與竇律患者相比,房顫患者KChIP2基因和Kv4.3基因明顯下調,KChIP2和Kv4.3基因下調是房顫時Ito電流下調的分子基礎.
목적 심방전동(방전)시최위상견적쾌속성심률실상지일.갑통도상관단백2(K+channel interacting protein 2,KChIP2)시심기세포순시외향갑통도적중요보조아단위,재,Ito발휘정상공능중기착중요적작용.보고채용실시형광정량취합매련반응(PCR)기술통과대방전시KChIP2화Kv4.3기인mRNA수평진행정량연구,탐토KChIP2재방전중적작용화대우순시외향갑통도적가능조공궤제.방법 (1)30례풍습성심장병환자분위량조:두성심률조(두률조)13례,지속성방전조(방전조)17례,취기상규절제적우심이조직작위연구대상;(2)제취심방기조직총RNA,통과RT-PCR화TA극륭기술구건함유목적 기인편단적질립표준품;(3)이GAPDH위내삼조기인,채용SYBR Green I법실시형광정량PCR기술검측지속성방전화두률환자KChIP2화Kv4.3기인mRNA수평.결과 (1)표준곡선화용해곡선:표준곡선선성관계량호,상관계수R2＞0.99.용해곡선정명현단봉상,퇴화온도여예측치기본일치;(2)두률조화방전조KChIP2/GAPDH비치분별위0.2200±0.0388、0.1468±0.0452,방전조KChIP2기인mRNA수평저우두률조,P＜0.01;두률조화방전조Kv4.3/GAPDH비치분별위0.5257±0.1427、0.3946±0.1826,방전조Kv4.3기인mRNA수평저우두률조,P＜0.05.결론 여두률환자상비,방전환자KChIP2기인화Kv4.3기인명현하조,KChIP2화Kv4.3기인하조시방전시Ito전류하조적분자기출.
Objectlve To detect the KChIP2 mRNA level in rheumatic heart disease patients with or without atrial fibrillation (AF) by real-time PCR.Methods Right atrial appendage samples from rheumatic heart disease patients with (n=17) or without AF (n=13) were obtained during cardiac surgery.Total RNA was extracted from the atrial tissues.and the KChIP2 and Kv4.3 mRNA were detected by SYBR Green I real-time PCR with the GAPDH as the house keeping gene.Result The ratio of KChIP2/GAPDH(0.1468 ±0.0452 VS.0.2200±0.0388,P＜0.01)and the ratio of Kv4.3/GAPDH(0.3946±0.1826 vs.0.5257±0.1427.P＜0.05)were significantly lower in AF patients compared to non-AF patients.Conclusion Down-regulated atrial KChIP2 and Kv4.3 mRNA expressions in rheumatic heart disease patients with chronic AF might be one of the molecular bases responsible for the down-regulation of the Ito current density of AF.
