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Rapid and marked induction of hepatocyte growth factor during liver regeneration after ischemic or crush injury
Author(s) -
Hamanoue Masahiro,
Kawaida Kouichi,
Takao Sonshin,
Shimazu Hisaaki,
Noji Sumihare,
Matsumoto Kunio,
Nakamura Toshikazu
Publication year - 1992
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840160626
Subject(s) - hepatocyte , hepatocyte growth factor , liver regeneration , liver injury , endocrinology , medicine , ischemia , biology , growth factor , gdf15 , in situ hybridization , regeneration (biology) , paracrine signalling , messenger rna , microbiology and biotechnology , biochemistry , in vitro , receptor , gene
Liver injuries induced by ischemia or physical trauma are characterized by noninflammatory damage frequently observed in a clinical setting. When the liver of rats was injured by ischemic treatment or physical crushing, necrotic tissue degeneration occurred in several sites of lobulus within 24 hr. Hepatocyte growth factor, a potent mitogen for adult rat hepatocytes in primary culture, was markedly induced in the livers of rats injured by ischemia or physical trauma. In both cases, the hepatocyte growth factor messenger RNA level in the injured liver reached about 10 to 20 times that of the normal level during 12 to 24 hr after liver injury. The increase in hepatocyte growth factor messenger RNA correlated well with the degree of liver damage as evaluated by serum ALT activity in the sera of rats. In situ hybridization showed that hepatocyte growth factor messenger RNA expression occurs in nonparenchymal liver cells, primarily in Kupffer cells of the ischemic liver. After the increase of hepatocyte growth factor messenger RNA in the injured liver, a marked compensatory hepatocyte DNA synthesis occurred 48 to 72 hr after these treatments. These results suggest that hepatocyte growth factor acts as a hepatotropic factor for liver regeneration after noninflammatory liver damage caused by ischemia and physical crush, probably through a paracrine mechanism.