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Role of Glucocorticoids and Resident Liver Macrophages in Induction of Tyrosine Aminotransferase

L. E. Panin* and I. F. Usynin

Institute of Biochemistry, Siberian Branch of the Russian Academy of Medical Sciences, ul. Akademika Timakova 2, 630117 Novosibirsk, Russia; fax: (3833) 356-811; E-mail: ibch@soramn.ru

* To whom correspondence should be addressed.

Received May 14, 2007; Revision received May 25, 2007
Administration of cortisol to an animal induces tyrosine aminotransferase (TAT) in the liver. A similar effect was observed after stimulation of resident liver macrophages (Kupffer cells) by dextran sulfate. Actinomycin D completely blocks enzyme induction both by cortisol and dextran sulfate, whereas their combined effect gives an additive result. In primary culture of hepatocytes, dextran sulfate inhibits TAT activity, but conditioned macrophage medium reliably increases enzyme activity in hepatocytes. However, incubation of isolated macrophages in the presence of dextran sulfate and such medium transfer into hepatocyte culture results in even more pronounced increase in TAT activity. In a combined culture of hepatocytes and non-parenchymal liver cells, reproducing intercellular interactions in vitro, cortisol and non-parenchymal cells exhibit an additive effect on TAT activity. These results show that liver macrophages release a factor of unknown nature launching the mechanism of TAT induction independently of cortisol, a classic TAT inducer.
KEY WORDS: tyrosine aminotransferase, glucocorticoids, macrophage, hepatocyte, liver, intercellular interactions, dextran sulfate

DOI: 10.1134/S0006297908030103