Itoh H, Koyata H, Takahara T, Watanabe A, Hiraga K
Department of Biochemistry, Toyama Medical and Pharmaceutical University School of Medicine, Japan.
Biochem Biophys Res Commun. 1992 Jun 30;185(3):981-6. doi: 10.1016/0006-291x(92)91723-4.
Northern analysis using total RNAs from the component cells of normal rat liver indicated that COL1A(I) mRNA is present in fat-storing cells (Ito cells) and sinusoidal endothelial cells. A fraction for Kupffer cells also contained this mRNA. When CCl4 was given, COL1A(I) mRNA was increased in a factor of 1.5 in the fractions of these component cells. After 48 h of the drug administration, hepatocytes appeared to possess over 60% of liver COL1A(I) mRNA, although in normal hepatocytes its level was below the range detectable by our procedures. Under this injured condition of liver, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA level was elevated, while activity of this enzyme was lowered by 50% of the control value. All the changes were obviously suppressed by the simultaneous administration of prostacyclin.
利用来自正常大鼠肝脏组成细胞的总RNA进行的Northern分析表明，Ⅰ型胶原（COL1AⅠ）mRNA存在于贮脂细胞（伊托细胞）和肝血窦内皮细胞中。库普弗细胞的一部分也含有这种mRNA。给予四氯化碳（CCl4）后，这些组成细胞部分中COL1AⅠmRNA增加了1.5倍。给药48小时后，肝细胞似乎占肝脏COL1AⅠmRNA的60%以上，尽管在正常肝细胞中其水平低于我们检测方法可检测的范围。在这种肝脏损伤状态下，甘油醛-3-磷酸脱氢酶（GAPDH）mRNA水平升高，而该酶的活性降低至对照值的50%。同时给予前列环素可明显抑制所有这些变化。
