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纤维连接蛋白及其受体在免疫性心肌炎小鼠心肌的表达(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第6期
页码:
626-630
栏目:
基础研究
出版日期:
2007-12-20

文章信息/Info

Title:
Expression of fibronectin and its receptor in mice experimental autoimmune myocarditis
作者:
吴辉; 唐其柱; 沈涤非; 卞洲艳; 熊然; 黄觊; 付金容; 魏小红
武汉大学人民医院心血管内科，湖北 武汉 430060
Author(s):
WU Hui;  TANG Qi-zhu;  SHEN Di-fei;  BIAN Zhou-yan;  XIONG Ran;  HUANG Ji;  FU Jin-rong;  WEI Xiao-hong
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, China
关键词:
自身免疫; 心肌炎; 纤维连接蛋白; CD29
Keywords:
Autoimmune;  Myocarditis;  Fibronectin;  CD29
分类号:
R542. 21
DOI:
-
文献标识码:
A
摘要:
目的 观察纤维连接蛋白（FN）及其受体CD29在实验性自身免疫性心肌炎（EAM）中的表达情况。方法 人工合成心肌肌球蛋白致病性抗原表位多肽，与弗氏完全佐剂(CFA)混合，在1d和8d免疫实验组小鼠（多肽剂量：100 μg /只），诱发EAM；对照组则给予PBS与CFA混合液。分别于21 d及75 d，检测心肌炎症评分、胶原容积分数（CVF）、Ⅲ型胶原（COLⅢ）mRNA的表达、FN及CD29的表达。结果 21 d时，实验组小鼠心肌炎性浸润明显，间质出现少量胶原沉积，COLⅢ mRNA、FN及CD29的表达均显著高于对照组(均P<0.01)。至75 d时，实验组小鼠心肌炎性浸润显著减少，间质胶原沉积更加明显，COLⅢ mRNA的表达进一步上调（P<0.05），FN的表达有所下降，CD29的表达则显著降低（P<0.01）,但仍显著高于对照组（P<0.01）。结论 在EAM时，FN及其受体在心肌的表达上调，可能参与了自身免疫性炎症损伤、组织修复及纤维化改变过程，从而促进心肌炎向心肌病的转化。
Abstract:
AIM To investigate the roles of fibronectin and its receptor CD29 in mice experimental autoimmune myocarditis (EAM). METHODS Polypeptides（myhcα614629） derived from cardiac myosin heavy chain were artificially synthesized and emulsified in Freund’s complete adjuvant (CFA). Genetically predisposed BALB/c mice were immunized with the emulsion on day 1 and day 8 and the control mice were immunized with mixture of PBS and CFA. A subset of mice was sacrificed respectively on day 21 and 75 after the first immunization, haematoxylin and eosin staining was used to identify areas of inflammation and Masson staining was used to identify areas of fibrosis. The relative gene expression level of collagenIII（COLⅢ） in myocardium was detected by reverse transcription polymerase chain reaction (RTPCR). The expression of fibronectin (FN) and CD29 in myocardium was assessed by immunohistochemistry staining. RESULTS On day 21 after the first immunization, the areas of inflammation, the relative gene expression level of COLⅢ in myocardium, the expression of FN and CD29 protein in experimental group were significantly higher than those in the control group(all P<0.01). On day 75, compared with those on day 21, the areas of inflammation infiltration (P<0.01) decreased, but the areas of fibrosis (P<0.01) enlarged significantly. The relative level of gene expression of COLⅢ(P<0.05) in myocardium increased significantly and the expression of FN and CD29(P<0.01) protein decreased, but still higher than those in the control group (P<0.01). CONCLUSION During the development of EAM in BALB/c mice, the expression of fibronectin and its receptor CD29 in myocardium increase and they may participate in the process of myocardium autoimmune inflammation, tissue repair and fibrosis changes, thus promoting the transformation of myocarditis to cardiomyopathy.

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备注/Memo

备注/Memo:
收稿日期：2006-11-27.通讯作者：唐其柱， 教授， 博导，主要从事心脏电生理、心肌疾病的发病机制与诊治的研究 Email: qizhut@yahoo.com.cn 作者简介：吴辉，医师，硕士 Email:whfly2001@tom.com.
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