Du W, Zhang Y, Ji X
Department of Pathology, Shanghai Medical University.
Zhonghua Yi Xue Za Zhi. 1997 Jul;77(7):513-5.
To investigate the synthesis and degradation of type IV collagen in CCl4-induced SD rat liver fibrosis.
Dynamic changes and relationships among the tissue alpha 1 (IV) procollagen mRNA, type IV collagen (Col IV) and serum 7S polypeptide fragment of Col IV in fibrotic livers induced by CCl4 with choline difficiency diet were studied using immunohistochemistry, Northern analysis, in situ hybridization and serum RIA techniques.
The transcription of alpha 1 (IV) procollagen mRNA in fibrotic liver and the content of serum 7S polypeptide fragment derived from tissue Col IV degradation was enhanced promptly and obviously in earlier stage of experiment, but not synchronous afterwards. In the early stage of experiment, alpha 1 (IV) procollagen mRNA transcripts was localized in sinusoid Ito cells and endothelial cells. In the mid and late stage, alpha 1 (IV) procollagen mRNA transcripts was localized in myofibroblasts (MFs), fibroblasts (Fbs) and endothelia of small blood vessels in fibrotic septa.
The change of serum 7S polypeptide fragment could reflect the motabolic state of Col IV and the degree of tissue injury in fibrogenesis and might have some clinical significance in identifying the activiation of the liver fibrosis. The "Ito cell-myofibroblast-fibroblast" effective cell system and sinusoid endothelia were the Col IV producing cells during fibrogenesis, in which sinusoid endothelia, as another source of Col IV production, participated in the capillization of liver sinusoids.
研究四氯化碳诱导的SD大鼠肝纤维化过程中IV型胶原的合成与降解。
采用免疫组织化学、Northern分析、原位杂交和血清放射免疫分析技术,研究在胆碱缺乏饮食条件下四氯化碳诱导的纤维化肝脏中组织α1(IV)前胶原mRNA、IV型胶原(Col IV)和血清Col IV 7S多肽片段的动态变化及相互关系。
实验早期,纤维化肝脏中α1(IV)前胶原mRNA的转录及组织Col IV降解产生的血清7S多肽片段含量迅速且明显升高,但随后不同步。实验早期,α1(IV)前胶原mRNA转录本定位于肝血窦Ito细胞和内皮细胞。实验中后期,α1(IV)前胶原mRNA转录本定位于肌成纤维细胞(MFs)、成纤维细胞(Fbs)以及纤维化间隔中小血管的内皮细胞。
血清7S多肽片段的变化可反映纤维化形成过程中Col IV的代谢状态及组织损伤程度,对判断肝纤维化的激活可能具有一定临床意义。“Ito细胞-肌成纤维细胞-成纤维细胞”有效细胞系统及肝血窦内皮细胞是纤维化形成过程中产生Col IV的细胞,其中肝血窦内皮细胞作为Col IV产生的另一个来源,参与了肝血窦的毛细血管化。