Kinoshita T, Tashiro K, Nakamura T
Department of Biology, Faculty of Science, Kyushu University, Fukuoka, Japan.
Biochem Biophys Res Commun. 1989 Dec 29;165(3):1229-34. doi: 10.1016/0006-291x(89)92733-2.
When experimental hepatitis was induced by administrating rats with hepatotoxins such as CCl4 and D-galactosamine, HGF mRNA increased dramatically in the injured liver. The increase of HGF mRNA was time- and dose-dependent. At 5 hr after CCl4-treatment, HGF mRNA was remarkably increased; it reached the maximum level at 10 hr and maintained at this level for 40 hr. On the contrary, in D-galactosamine-induced hepatitis, HGF mRNA started to increase from 24 hr after a long lag time. Moreover, HGF mRNA was expressed transiently, decreasing rapidly to the basal level after reaching the maximum level at 36 hr. The degree of induction of HGF mRNA correlates well to the degree of liver damage. In the liver, HGF mRNA could be detected in only non-parenchymal cells, not in parenchymal hepatocytes. These findings suggest that liver is a main producing organ of HGF for liver regeneration after hepatic injury, and HGF is synthesized and secreted by non-parenchymal liver cells so that it stimulates the growth of parenchymal hepatocytes to repair liver tissue in paracrine fashion.
当通过给大鼠施用四氯化碳（CCl4）和D-半乳糖胺等肝毒素诱导实验性肝炎时，受损肝脏中肝细胞生长因子（HGF）mRNA显著增加。HGF mRNA的增加具有时间和剂量依赖性。在CCl4处理后5小时，HGF mRNA显著增加；在10小时达到最高水平，并在此水平维持40小时。相反，在D-半乳糖胺诱导的肝炎中，经过较长的延迟时间后，HGF mRNA从24小时开始增加。此外，HGF mRNA短暂表达，在36小时达到最高水平后迅速降至基础水平。HGF mRNA的诱导程度与肝损伤程度密切相关。在肝脏中，仅在非实质细胞中可检测到HGF mRNA，而在实质肝细胞中未检测到。这些发现表明，肝脏是肝损伤后肝再生的HGF主要产生器官，并且HGF由肝脏非实质细胞合成和分泌，从而以旁分泌方式刺激实质肝细胞生长以修复肝组织。
