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METHOD FOR MEASUREMENT OF CELL PROLIFERATION INHIBITING FACTOR IN HEART

心脏细胞增殖抑制因子的测定方法

基本信息

批准号：
03557038
负责人：
KAWAGUCHI Hideaki
金额：
$ 8.96万
依托单位：
HOKKAIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B).
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-03557038/
关键词：
CARDIOMYOPATHY COLLAGEN FIBROSIS REMODELING EXTRACELLULAR MATRIX PI-PLC IP3 TGFβ C-myc oncogene 細胞増殖因子 DNA 心筋細胞遺伝子

项目摘要

Extensive fibrosis is remarkable in cardiomyopathy. The purpose of this study is to characterize the collagen, one of the chief elements of the extracellular matrix of hereditarycardiomyopathic hamsters, and to examine the participation of the collagen in the occurrence and the progression of the cardiomyopathy. BIO53.58(5,11,22 weeks) was used as the model of the dilated cardiomyopathy and BIO14.6 (20,30 weeks) was used as the model of the hypertrophic cardiomyopahty. F1b was used as the control. The collagen content was almost constant at any age in F1b, but increased with aging in BIO53.58 and BIO14.6. Type III collagen increased significantly in BIO53.58 at 11 weeks and BIO14.6 at 20 weeks. Type V collagen decreased significantly in BIO14.6 at 30 weeks. Aceticacid solubility of collagen decreased in BIO53.58 and BIO14.6 with the progression of the fibrosis, but not in F1b. Reducible crosslinks showed the tendency to decrease in BIO53.58 progressively. Histologicallythick collagen fiber increased in BIO53.58 and BIO14.6. These findings indicate that in the early phase of the cardiomyopathy the extracellular matrix of the myocardium has characteristics that of the immature tissues which are rich in type III collagen. In later phase, the matrix resembles that of hard tissues whose collagen is mainly of type Icollagen and have low solubility. It is considered that the increase of the thick collagen fiber combined firmly in heart may affect the diastolicand the systolic function in addition to the loss of the cardiac muscle fiber by the deg eneration and the necrosis.

广泛性纤维化在心肌病中是显著的。本研究的目的是研究遗传性心肌病仓鼠细胞外基质的主要成分之一胶原的特性，并探讨胶原在心肌病发生和发展中的作用。以BIO53.58（5、11、22周）为扩张型心肌病模型，BIO14.6（20、30周）为肥厚型心肌病模型。F1b作为对照。在F1b中，胶原蛋白含量在任何年龄都几乎恒定，但在BIO53.58和BIO14.6中，胶原蛋白含量随着年龄的增长而增加。11周时BIO53.58和20周时BIO14.6中的III型胶原蛋白显着增加。在30周时，BIO14.6中的V型胶原显著减少。在BIO53.58和BIO14.6中，胶原的乙酸溶解度随着纤维化的进展而降低，而在F1b中则没有。在BIO53.58中，可还原交联显示出逐渐降低的趋势。BIO53.58和BIO14.6中组织学上厚的胶原纤维增加。这些发现表明，在心肌病的早期阶段，心肌细胞外基质具有富含III型胶原的未成熟组织的特征。后期基质类似硬组织，胶原主要为I型胶原，溶解度低。认为心脏内结合牢固的粗胶原纤维增多，除了使心肌纤维变性坏死而丧失外，还可能影响到收缩和舒张功能。