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目的探讨心脏瓣膜病(瓣膜病)慢性房颤患者左右心房肌间质纤维化的分子生物学机制是否存在差异。方法接受开胸换瓣的手术患者45例,慢性房颤患者27例,窦性心律患者18例,术中分别取左、右心耳组织,采用半定量逆转录-聚合酶链反应(RT-PCR)测定I型胶原、III型胶原、基质金属蛋白酶-1、9(MMP1、MMP9)以及基质金属蛋白酶抑制剂-1(TMP1)的mRNA表达水平。结果①与窦性心律组相比,慢性房颤组患者左、右心房肌组织中I型胶原、MMP1、MMP9的mRNA表达水平均上调(P<0.05),TMP1的表达水平均下调(P<0.01)。②窦性心律组患者左右心房肌组之间I型胶原、III型胶原、MMP1、MMP9、TMP1的mRNA表达水平差异均无显著性(P>0.05)。③慢性房颤组患者MMP1的mRNA在右心房肌组织中表达水平较左心房上调(P<0.05),MMP9的mRNA在左心房肌组织中表达水平较右心房上调(P<0.01)。④无论左心房还是右心房,MMP1、MMP9的mRNA表达水平均与I型胶原的mRNA表达水平呈正相关,与TMP1的mRNA表达水平呈负相关。结论心房肌组织中MMP1/TMP1以及MMP9/TMP1的mRNA表达水平失衡引起I型胶原转录水平的改变,可能是瓣膜病慢性房颤患者心房肌间质纤维化的分子基础,而左、右心房间质纤维化是被MMP1和MMP9差异化调控的。
Objective To investigate the molecular mechanisms of left and right atrial interstitial fibrosis in patients with chronic valvular heart disease (valvular disease). Methods Forty-five patients with open thoracostomy, 27 patients with chronic atrial fibrillation and 18 patients with sinus rhythm were included. Left and right atrial appendage tissues were obtained and semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) ) Were used to determine the mRNA expression levels of type I collagen, type III collagen, matrix metalloproteinase-1, 9 (MMP1, MMP9), and matrix metalloproteinase inhibitor-1 (TMP1) Results ① Compared with sinus rhythm group, the mRNA expression of type I collagen, MMP1 and MMP9 in left and right atria of chronic atrial fibrillation group were increased (P <0.05) and TMP1 expression level was decreased (P < 0.01). ② There was no significant difference in mRNA expression of type I collagen, type III collagen, MMP1, MMP9 and TMP1 between the left and right atrium muscles in patients with sinus rhythm (P> 0.05). ③The expression of MMP1 mRNA in the right atrial myocardium in chronic atrial fibrillation group was higher than that in the left atrium (P <0.05). The mRNA expression of MMP9 was up-regulated in the left atrial muscle tissue compared with the right atrium (P <0.01). ④ Whether left atrium or right atrium, MMP1, MMP9 mRNA expression levels were positively correlated with type I collagen mRNA expression, and TMP1 mRNA expression level was negatively correlated. Conclusion The imbalanced mRNA expression of MMP1 / TMP1 and MMP9 / TMP1 in atrial myocardium may cause the change of type I collagen transcription, which may be the molecular basis of atrial fibrosis in patients with valvular atrial fibrillation. Fibrosis is differentially regulated by MMP1 and MMP9.