SOLUBLE INTERLEUKIN 6 (IL-6) RECEPTOR INFLUENCES THE EXPRESSION OF THE PROTOONCOGENE junB AND THE PRODUCTION OF FIBRINOGEN IN THE HepG2 HUMAN HEPATOMA CELL LINE AND PRIMARY RAT HEPATOCYTES

• Published in: Cytokine (Philadelphia, Pa.) Vol. 10; no. 8; pp. 620 - 626
• Main Authors: Igaz, Peter, Tóth, Sara, Rose-John, Stefan, Madurka, Ildikó, Fejér, György, Szalai, Csaba, Falus, Andras
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.1998
• Subjects: Animals; Carcinoma, Hepatocellular; Cells, Cultured; fibrinogen; Fibrinogen - biosynthesis; Gene Expression Regulation; hepatocytes; Humans; interleukin 6; junB; Liver - cytology; Liver - metabolism; Polymerase Chain Reaction - methods; Proto-Oncogene Proteins c-jun - biosynthesis; Proto-Oncogene Proteins c-jun - genetics; Rats; Receptors, Interleukin-6 - metabolism; RNA, Messenger; Solubility; soluble receptor; Tumor Cells, Cultured; interleukin 6; fibrinogen; soluble receptor; hepatocytes; junB
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1006/cyto.1997.0330

Interleukin 6 (IL-6) belongs to a family of cytokines using receptors sharing a common signal-transducing chain, gp130 and containing a specific ligand-binding chain (IL-6Rα). It was shown that both the membrane-bound and the soluble form (sIL-6R) of this ligand specific receptor chain occurs naturally. The soluble form of IL-6 receptor was found to be able to associate with the membrane-bound gp130 and to generate active IL-6 receptor complex capable of inducing signal transduction. This study on a human hepatoma cell line and primary rat hepatocytes examined how the effectiveness of IL-6 is modified by the presence of soluble IL-6 receptor and whether the sIL-6R in the absence of IL-6 acts on hepatocytes. The authors studied the gene expression ofJunB, a member of the Jun family of transcription factors, and the production of fibrinogen in response to IL-6 and sIL-6R. The data show that the hepatic cells, endogeneously expressing IL-6R, the IL-6 induced junB and fibrinogen expression is inhibited by the presence of sIL-6R. In addition we found that sIL-6R alone (in the absence of IL-6) induced junB mRNA expression, but had no effect on fibrinogen production.