[基质金属蛋白酶-1、金属蛋白酶组织抑制因子-1及转化生长因子-β1在风湿性心脏病瓣膜组织中的意义及表达]

[Significance and Expressions of MMP-1, TIMP-1 and TGF-β1 in Valve Tissue of Rheumatic Heart Disease].

作者信息

Yu Yi, Li Zeng-Qi, Chen Kun, Zhan Ping, Liao Jian, Ruan Qin-Yun

机构信息

Department of Cardiac Surgery, the First Affiliated Hospital of Fujian Medical University, Fuzhou 350004, China.

Department of Ultrasonography, the First Affiliated Hospital of Fujian Medical University, Fuzhou 350004, China.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2017 Jan;48(1):52-56.

PMID:28612558

Abstract

OBJECTIVES

To explore expressions of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinases-1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in valve tissue of rheumatic heart disease (RHD), and to analyzed their roles in RHD.

METHODS

The expressions of MMP-1, TIMP-1 and TGF-β1 proteins and mRNAs were tested by Western blot and RT-PCR methods in valve tissues in participants with (experimental group, =30) and without RHD (control group, =15). Collagen fibers were detected by Masson staining, and collagen volume fraction (CVF) was caculated. The correlations of CVF and the expressions of MMP-1, TIMP-1 and TGF-β1 were analyzed.

RESULTS

The collagen fibers, CVF, and the protein and mRNA expressions of MMP-1 and TGF-β1 in experimental group were higher than those in control group, while the protein and mRNA expressions of TIMP-1 in experimental group were lower than those in control group. The expression of TIMP-1 was negatively correlated with TGF-β1 and CVF in valve tissues, while MMP-1 was positively correlated with them. The expression of TGF-β1 was positively correlated with CVF in valve tissues.

CONCLUSIONS

MMP-1, TIMP-1 and TGF-β1 contribute to the progression of fibrosis in RHD.

摘要

目的

探讨基质金属蛋白酶-1（MMP-1）、金属蛋白酶组织抑制剂-1（TIMP-1）和转化生长因子-β1（TGF-β1）在风湿性心脏病（RHD）瓣膜组织中的表达，并分析它们在RHD中的作用。

方法

采用蛋白质印迹法和逆转录-聚合酶链反应（RT-PCR）法检测30例RHD患者（实验组）和15例非RHD患者（对照组）瓣膜组织中MMP-1、TIMP-1和TGF-β1蛋白及mRNA的表达。采用Masson染色检测胶原纤维，并计算胶原容积分数（CVF）。分析CVF与MMP-1、TIMP-1和TGF-β1表达的相关性。