L及T型钙离子通道α1亚基在风湿性房颤心房组织中的表达变化

Changes of the mRNA and protein expression of α1 subunit of L-type and T-type calcium channels in human atrial myocardium of rheumatic atrial fibrillation patients

目的研究正常窦律(NSR)、风湿性瓣膜病窦律(RSR)及风湿性瓣膜病房颤(RAF)三组患者右房组织中L型钙离子通道α1C和T型钙离子通道α1G、α1H亚基mRNA及蛋白的表达差异。方法术中获取各组患者(NSR=10,RSR=11,RAF=16)少量右房标本,实时荧光定量RT-PCR对各组α1C、α1G及α1H亚基的mRNA丰度相对定量(2-ΔΔCt法);蛋白免疫印迹法比较三种α1亚基蛋白表达水平。结果与NSR及RSR组相比,RAF组的α1C及α1H的mRNA丰度及蛋白水平显著上调(P<0.05),α1G表达水平三组间差异不显著;三种α1亚基在NSR及RSR两组间表达水平无显著差异。结论房颤时,α1C及α1H亚基表达水平上调,而α1G亚基表达水平不变;风湿性因素对L及T型钙离子通道的表达并无直接影响,但不能排除其对钙离子通道功能发生影响的可能。

Objective To investigate whether there are changes in the expression,at mRNA and protein level,of α1 subunits of L-type （α1C） and T-type （α1G andα1H） calcium channels in the human atrial myocardium among normal sinal rhythm （NSR）,rheumatic sinal rhythm （RSR） and rheumatic atrial fibrillation （RAF） patients.Methods The right atrial tissue was obtained from three distinct groups of patients during the cardiac surgeries,and the numbers of the patient were 10 for NSR,11 for RSR,and 16 for RAF,respectively.Real-time quantative RT-PCR was used to measure the abundance of mRNA of three different calcium channel α1 subunits （CACNA1C,CACNA1G,CACNA1H） by the 2-Ct method.Western Blot was also used to examine the expression of these three channel proteins by a semi-quantative method.Results In comparison with the NSR and RSR groups,the mRNA abundance and protein expression level of α1C and α1H subunits was significantly up-regulated in the RAF group （P0.05）.However,the level of α1G subunit was not significantly different among the three groups.Between the NSR and RSR groups,there were no significant differences of the expression of all three subunits.Conclusions The present study demonstrated that the expression of α1C and α1H subunits,but not α1G subunit,was up-regulated in atrial fibrillation,suggesting rheumatics may not affect the expression level of L-type and T-type calcium channel.Whether the rheumatics might still change calcium channel functions remains elusive.