慢性心房颤动心房肌间质纤维化的分子机制研究
The molecular mechanism of atrial interstitial fibrosis in patients with chronic atrial fibrillation
目的 研究心脏瓣膜病慢性心房颤动(房颤)患者心房肌间质纤维化的分子生物学机制.方法心脏瓣膜病接受瓣膜置换手术患者45例,慢性房颤27例,窦性心律18例,手术中取右心耳组织,采用半定量逆转录-聚合酶链反应测定Ⅰ型胶原、Ⅲ型胶原、基质金属蛋白酶(MMPs)中胶原酶(MMP1、MMP8、MMP13)以及基质金属蛋白酶抑制剂(TIMPs)中TMP1、TMP2、TMP3、TMP4的mRNA表达水平.结果 (1)与窦性心律组比较,慢性房颤组Ⅰ型胶原、MMP13、MMP1的mRNA表达上调(P<0.05),TMP1、TMP2、TMP3的mRNA表达下调(P<0.05).(2)MMP1的mRNA表达与Ⅰ型胶原的mRNA表达、左心房内径呈正相关,与TMP1的mRNA表达呈负相关.MMP13的mRNA表达与Ⅰ型胶原的mRNA表达、左心房内径呈正相关,与TMP3的mRNA表达呈负相关.结论 慢性房颤患者心房肌组织中MMP1/TMP1以及MMP13/TMP3的基因转录表达水平失衡引起Ⅰ型胶原转录水平的改变,可能是慢性房颤患者心房肌间质纤维化的分子基础.
更多Objective To evaluate the molecular mechanisms of atrial interstitial fibrosis in patients with chronic atrial fibrillation(AF). Methods The right atrial appendages were obtained from 45 patients with valvular heart disease who underwent heart valvular replacement surgery. 18 patients were in sinus rhythm,27 patients were in chronic atrial fibrillation. The mRNA level of collagen type Ⅰ, collagen type Ⅲ, MMP1, MMP8, MMP13, TMP1, TMP2, TMP3, TMP4 were measured by semi-quantitative reverse transcription-polymer-ase chain reaction (RT-PCR). Results (1) Compared with the sinus rhythm group, in chronic AF group, the mRNA of collagen type Ⅰ, MMP1, and MMP13 increased (P<0.05),while the mRNA of TMP1, TMP2, TMP3 significantly decreased (P<0.05). (2)The mRNA level of MMPI was significantly correlated with the mRNA level of collagen type Ⅰ and left atial dimension. The mRNA level of MMP1 was negatively correlated with the mRNA level of TMP1. The mRNA level of MMP13 was significantly correlated with the mRNA level of collagen type Ⅰ and left atial dimension. The mRNA level of MMP13 was negatively correlated with the mRNA level of TMP3. Conclusion The increased level of collagen type Ⅰ associated with selective upregulation of MMP1,13 and downregulation of TMP1,3 gcne expression in atrium might be the molecular basis of atrial interstitial fibro-sis in patients with chronic atrial fibrillation.
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