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J. Biol. Chem., Vol. 280, Issue 40, 33856-33863, October 7, 2005

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Cross-talk among gp130 Cytokines in Adipocytes^*

Sanjin Zvonic, James E. Baugh, Jr., Patricia Arbour-Reily, Randall L. Mynatt, and Jacqueline M. Stephens1

From the Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana 70803 and Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808

The interleukin-6 (IL-6) family of cytokines is a family of structurally and functionally related proteins, including IL-6, IL-11, leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1). These proteins are also known as gp130 cytokines because they all share gp130 as a common transducer protein within their functional receptor complexes. Several of these cytokines (LIF, OSM, CNTF, and CT-1) also utilize the LIF receptor (LIFR) as a component of their receptor complex. We have shown that all of these cytokines are capable of activating both the JAK/STAT and p42/44 mitogen-activated protein kinase signaling pathways in 3T3-L1 adipocytes. By performing a variety of preincubation studies and examining the ability of these cytokines to activate STATs, ERKs, and induce transcription of SOCS-3 mRNA, we have also examined the ability of gp130 cytokines to modulate the action of their family members. Our results indicate that a subset of gp130 cytokines, in particular CT-1, LIF, and OSM, has the ability to impair subsequent signaling activity initiated by gp130 cytokines. However, IL-6 and CNTF do not exhibit this cross-talk ability. Moreover, our results indicate that the cross-talk among gp130 cytokines is mediated by the ability of these cytokines to induce ligand-dependent degradation of the LIFR, in a proteasome-independent manner, which coincides with decreased levels of LIFR at the plasma membrane. In summary, our results demonstrate that an inhibitory cross-talk among specific gp130 cytokines in 3T3-L1 adipocytes occurs as a result of specific degradation of LIFR via a lysosome-mediated pathway.

Received for publication, July 22, 2005

^* This work was supported by Grant R01DK52968-02 from the National Institutes of Health (to J. M. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Biological Sciences, Lousisiana State University, 202 Life Sciences Bldg., Baton Rouge, LA 70803. Tel.: 225-578-1749; Fax: 225-578-2597; E-mail: jsteph1{at}lsu.edu.

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