| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
In the conditioned medium (CM) of an HTLV-I(+) T cell line, ATL-2, we have detected a cytokine that dose-dependently inhibits the epidermal growth factor (EGF)-dependent proliferation of primary cultured rat hepatocytes. Both the increase of cell number and @[^3H]-thymidine incorporation of the hepatocytes were similary inhibited by the addition of this CM. This hepatocyte growth inhibitory factor (HGI) was fractionated at the molecular size of 15,000 to 40,000 using a Sephacryl S-200 column. While the activity of an interleukin-2 (IL-2) receptor inducing factor derived from the same CM, ADF, was overlapping with HGI, further fractionation with ion-exchange column indicated that HGI was different from ADF. However, other HTLV-I transformed T cell lines also co-produced HGI and ADF, suggesting a positive correlation between HGI and ADF. Lymphokines such as IL-2, interleukin-1 (IL-1 ) and interferon- (IFN- ) did not affect hepatocyte proliferation. Because transforming growth factor- (TGF- ) showed a significant inhibitory activity to hepatocyte proliferation, we discuss the relationship between HGI and TGF- . The results suggested that HGI may be involved in the pathophysiology of liver dysfunction of ATL patients and/or in the ragulation of liver rageneration.
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