摘要
目的探讨心房颤动(简称房颤)患者心房肌电和结构重构以及心功能下降的分子生物学机制。方法采集风湿性心脏瓣膜病(简称风心病)窦性心律患者12例(窦律组)和房颤患者16例(房颤组)的右心耳组织,应用半定量逆转录-聚合酶链反应方法,测定心房肌钙转运调控蛋白和钙激活中性蛋白酶(calpain1)的mRNA表达水平。结果与窦律组比较,房颤组L-型电压依赖钙通道a1c亚基(LVDCCa1c)、肌浆网Ca2+-ATP酶、兰尼碱受体的mRNA表达水平显著下调(P均<0.01),三磷酸肌醇受体的mRNA表达水平上调(P<0.05);房颤组心房肌cal-pain1的mRNA表达水平上调(P<0.05),且与LVDCCa1c的mRNA表达呈负相关(r=-0.583,P=0.019)。结论房颤患者心房肌钙转运调控蛋白和calpain1转录水平调控失衡可能是心房肌电和结构重构以及心功能下降的分2子生物学机制之一。
Objective To evaluate the molecular mechanisms of atrial fibrillation （AF） . Methods The right atrial appendages were obtained from 16 patients with atrial fibrillation （cases） and from 12 matched controls with sinus rhythm. The mRNA expression of proteins influencing the calcium homeostasis and atrial calpainl was measured by semi-quantitative reverse transcription-polymerase chain reaction and noralalized to the mRNA level of glyceraldehyde-3-phosphate dehydrogenase. Results Compared to the sinus rhythm group, the mRNA level of calpainl was significantly increased（P 〈0.05 ）, while the mRNA level of L-type calcinm channel alc（ LVDCCal c ） was significantly decreased（ P 〈0.01 ）. The mRNA level of LVDCCal c was negatively correlated with calpainl （r = -0. 583, P = 0. 019 ）. Compared to sinus rhythm group, the mRNA levels of sarcoplaslnic reticulum calcium adenosine triphosphatase and ryanodine receptor type-2 were significantly decreased（ P 〈 0.01 ） , but the mRNA level of inositol triphosphate receptor type-1 was significantly increased（P 〈 0. 05 ）. Conclusion Chronic AF is predominantly accompanied bv abnormal regulation in the mRNA expression influencing the calcium homeostasis and atrial calpainl , which are related to both electrical remolding and structural changes.
出处
《中国心脏起搏与心电生理杂志》
2007年第6期500-503,共4页
Chinese Journal of Cardiac Pacing and Electrophysiology
基金
新疆维吾尔自治区高校科研计划科学研究优秀青年学者奖励计划项目(项目编号:XJEDU2004E10)
