Relationship Between Atrial MMP-9/TIMP-1 With Apoptosis Related Gene and Aging With Atrial Fibrillation in Experimental Dog Model
10.3969/j.issn.1000-3614.2014.12.018
- VernacularTitle:心房肌基质金属蛋白酶及其抑制剂、凋亡相关基因表达改变与增龄性心房颤动关系的研究
- Author:
Lijun DONG
;
Baopeng TANG
;
Xianhui ZHOU
;
Jinxin LI
;
Yu ZHANG
;
Ling SUN
;
Yaodong LI
;
Jianghua ZHANG
;
Qiang XING
;
Guojun XU
- Publication Type:Journal Article
- Keywords:
Atrial ifbrillation;
Aging;
Atrial remodeling;
Atrial ifbrosis;
Apoptosis
- From:
Chinese Circulation Journal
2014;(12):1034-1038
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the relationship between atrial MMP-9 with its inhibitor (TIMP-1), anti-apoptosis gene (BCL-2) with apoptosis gene (BAX) and the aging with atrial remodeling in experimental dog model during atrial ifbrillation (AF), in order to better deal with the aging caused AF.
Methods: The experimental dogs were divided into 4 groups: ①Adult with sinus rhythm (ASR) group, ②Elder with sinus rhythm (ESR) group and③Adult with AF (AAF) group,④Elder with AF (EAF) group. n=7 in each group. Chronic AF model was induced by rapid and persistent atrial pacing. The mRNA and protein expressions of MMP-9, TIMP-1 and BCL-2, BAX were measured by real time quantitative RT-PCR and Western blot analysis. The cellular ultra structural remodeling was examined by optical/electron microscopy, and the apoptosis index was determined by TUNEL method,
Results: Compared with adult dogs, the elder dogs showed obviously increased expressions of MMP-9, BAX, and decreased expressions of TIMP-1, BCL-2, all P<0.05. Compared with SR gods, the AF dogs presented up-regulated expressions
of MMP-9, BAX, all P<0.05, and down-regulated expressions of TIMP-1, BCL-2, all P<0.05, such changes were most obvious in elder AF dogs. Accompanying with the aging and AF, the degree of atrial ifbrosis, cellular ultra structure and the apoptosis index were changed with the statistic meaning.
Conclusion: The abnormal expressions of MMP-9/TIMP-1 and BCL-2/BAX might be one of the molecular mechanisms for aging caused AF in experimental dog model.
