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实验性自身免疫性心肌炎Lewis大鼠心脏中小窝蛋白-1和-2的表达增加。

Increased expression of caveolin-1 and -2 in the hearts of Lewis rats with experimental autoimmune myocarditis.

作者信息

Ahn Meejung, Kim Heechul, Matsumoto Yoh, Shin Taekyun

机构信息

Department of Veterinary Medicine, Graduate School, Cheju National University, Jeju City, 690-756, South Korea.

出版信息

Autoimmunity. 2006 Sep;39(6):489-95. doi: 10.1080/08916930600929321.

DOI:10.1080/08916930600929321
PMID:17060028
Abstract

The expression of caveolin-1, -2 and -3 was studied in the hearts of rats with experimental autoimmune myocarditis (EAM), to elucidate the involvement of caveolins in the pathogenesis of EAM. Western blot analysis showed that levels of caveolin-1 and -2 were significantly increased in the hearts of rats with EAM on day 14 post-immunization (pi), as compared to the hearts of normal controls (p < 0.05, normal controls vs. EAM). Caveolin-3 is already at a high level in control animals, so it does not increase further. Immunohistochemistry showed that caveolin-1 was expressed mainly in ED1-positive macrophages and in some cardiomyocytes and vessels in the EAM lesions. Caveolin-2 was expressed constitutively in the vascular endothelial cells of normal hearts, and its expression was enhanced in EAM rats, as compared with the normal control group. Caveolin-3 was expressed constitutively in the plasma membranes of cardiomyocytes, but not in the vascular endothelial cells and inflammatory cells in the EAM lesions. Our results suggest that the expression of caveolin-1 and -2 is increased in EAM lesions and that the increased expression of caveolin-1 stimulates second signals in affected cells, such as macrophages and some cardiomyocytes, in EAM rats.

摘要

研究了实验性自身免疫性心肌炎(EAM)大鼠心脏中小窝蛋白-1、-2和-3的表达,以阐明小窝蛋白在EAM发病机制中的作用。蛋白质印迹分析表明,与正常对照大鼠心脏相比,免疫接种后14天EAM大鼠心脏中小窝蛋白-1和-2的水平显著升高(p < 0.05,正常对照vs. EAM)。小窝蛋白-3在对照动物中已处于高水平,因此其水平不再进一步升高。免疫组织化学显示,小窝蛋白-1主要在EAM病变中的ED1阳性巨噬细胞以及一些心肌细胞和血管中表达。小窝蛋白-2在正常心脏的血管内皮细胞中组成性表达,与正常对照组相比,其在EAM大鼠中的表达增强。小窝蛋白-3在心肌细胞质膜中组成性表达,但在EAM病变中的血管内皮细胞和炎性细胞中不表达。我们的结果表明,EAM病变中小窝蛋白-1和-2的表达增加,并且小窝蛋白-1表达的增加在EAM大鼠的受影响细胞(如巨噬细胞和一些心肌细胞)中刺激第二信号。

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