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1 Johns Hopkins University, Baltimore, Maryland 21205; and 2 Hennepin County Medical Center, Minneapolis, Minnesota 55415
Ethanol ingestion may interrupt the
proregenerative signal transduction that is initiated by injury-related
cytokines such as tumor necrosis factor (TNF)-
and TNF--
inducible cytokines including interleukin (IL)-6. To test this theory,
liver regeneration, TNF- and IL-6 expression, and cytokine-regulated
prereplicative events were compared in ethanol-fed rats and
isocalorically fed controls after 70% partial hepatectomy (PH).
Ethanol feeding inhibits hepatocyte replication and recovery of liver
mass after PH but generally promotes induction of both cytokines in the
liver and extrahepatic tissues (i.e., white adipose tissue).
Cytokine-regulated events that occur early in the prereplicative period
are influenced differentially. TNF--dependent increases in hepatic
nuclear factor-
B (NF-B) p50 and p65 expression and DNA binding
activity are prevented, whereas IL-6-dependent inductions of hepatic
Stat-3 phosphorylation and DNA binding activity occur normally. In
contrast, events (e.g., induction of cyclin D1, cdk-1, cyclin D3, and
p53 mRNA) that occur at the end of the prereplicative period are
uniformly inhibited. These findings indicate that chronic ethanol
ingestion arrests the regenerative process during the prereplicative
period and demonstrate that increased TNF-, IL-6 and Stat-3 are not
sufficient to assure hepatocyte proliferation after PH.
tumor necrosis factor; interleukin-6; Stat-3; transcription factors; adipose tissue
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