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.
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Dec 30 1989|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology