TY - JOUR
T1 - Marked increase of HGF mRNA in non-parenchymal liver cells of rats treated with hepatotoxins
AU - Kinoshita, Taisei
AU - Tashiro, Kosube
AU - Nakamura, Toshikazu
N1 - Funding Information:
This work was supported by a Research Grant for Science and Cancer from Ministry of Education and Culture of Japan, and Research Grants from the Princes Takamatsu Cancer Research Fund, the Cell Science Research Foundation. and the Terumo Life Science Foundation.
PY - 1989/12/30
Y1 - 1989/12/30
N2 - 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.
AB - 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.
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U2 - 10.1016/0006-291X(89)92733-2
DO - 10.1016/0006-291X(89)92733-2
M3 - Article
C2 - 2692563
AN - SCOPUS:0024788217
SN - 0006-291X
VL - 165
SP - 1229
EP - 1234
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -
