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目的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,探讨风湿性心脏瓣膜病(风心病)心房颤动(房颤)患者心房肌电重构和结构重构以及心功能下降的分子生物学机制及其在房颤发生、维持中的作用。方法采集风心病窦性心律组患者12例和房颤组患者16例的右心耳组织,应用半定量逆转录-聚合酶链反应(RT-PCR)方法,测定心房肌钙转运调控蛋白和calpain1的mRNA表达水平。结果与窦性心律组相比,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(RYR2)的mRNA表达水平明显下调(均为P<0.01),三磷酸肌醇受体(IP3R1)的mRNA表达水平上调(P<0.05),房颤组心房肌calpain1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<0.05)。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重构和结构重构以及心功能下降的分子生物学机制之一,与房颤的发生和维持有关。
Aim To determine the mRNA expression of calmodulin and calpain1 in atrial fibrillation and to investigate the changes of atrial and cardiac electrical remodeling and cardiac remodeling in atrial fibrillation patients with rheumatic valvular heart disease (rheumatic heart disease) Decline in molecular biology and its mechanism in the occurrence and maintenance of atrial fibrillation. Methods The right atrial appendages were collected from 12 patients with sinus rhythm of rheumatic heart disease and 16 patients with atrial fibrillation. The expressions of calcium transport regulatory protein and calpain 1 in atrial fibrillation were determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) mRNA expression level. Results Compared with sinus rhythm group, L-type voltage-dependent L-type voltage-dependent calcium channel a1c subunit (LVDCCa1c), sarcoplasmic reticulum Ca2 + -ATPase and RANR2 mRNA expression were significantly decreased (P <0.01). The mRNA expression of inositol 1,4,5-trisphosphate receptor (IP3R1) was up-regulated (P <0.05), and the mRNA expression of calpain1 in atrial fibrillation group was up-regulated Negative correlation (r = -0.583, P <0.05). Conclusions The imbalance of atrial calcium transport regulatory protein and calpain1 transcriptional regulation in atrial fibrillation patients may be one of the molecular mechanisms of atrial myoelectrical remodeling and structural remodeling as well as cardiac dysfunction, which is related to the occurrence and maintenance of atrial fibrillation.