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Originally published In Press as doi:10.1074/jbc.M009147200 on February 2, 2001

J. Biol. Chem., Vol. 276, Issue 17, 13771-13777, April 27, 2001
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Tumor Necrosis Factor-alpha Induction of Endothelial Ephrin A1 Expression Is Mediated by a p38 MAPK- and SAPK/JNK-dependent but Nuclear Factor-kappa B-independent Mechanism*

Nikki ChengDagger and Jin ChenDagger §

From the Dagger  Department of Cell Biology and the § Division of Rheumatology and Department of Medicine, Vanderbilt University Medical School, Nashville, Tennessee 37232

Tumor necrosis factor-alpha (TNF-alpha ) is a multifunctional cytokine that induces a broad spectrum of responses including angiogenesis. Angiogenesis promoted by TNF-alpha is mediated, at least in part, by ephrin A1, a member of the ligand family for Eph receptor tyrosine kinases. Although TNF-alpha induces ephrin A1 expression in endothelial cells, the signaling pathways mediating ephrin A1 induction remain unknown. In this study, we investigated the signaling mechanisms of TNF-alpha -dependent induction of ephrin A1 in endothelial cells. Both TNFR1 and TNFR2 appear to be involved in regulating ephrin A1 expression in endothelial cells, because neutralizing antibodies to either TNFR1 or TNFR2 inhibited TNF-alpha -induced ephrin A1 expression. Inhibition of nuclear factor-kappa B (NF-kappa B) activation by a trans-dominant inhibitory isoform of mutant Ikappa Balpha did not affect ephrin A1 induction, suggesting that NF-kappa B proteins are not major regulators of ephrin A1 expression. In contrast, ephrin A1 induction was blocked by inhibition of p38 mitogen-activated protein kinase (MAPK) or SAPK/JNK, but not p42/44 MAPK, using either selective chemical inhibitors or dominant-negative forms of p38 MAPK or TNF receptor-associated factor 2. These findings indicate that TNF-alpha -induced ephrin A1 expression is mediated through JNK and p38 MAPK signaling pathways. Taken together, the results of our study demonstrated that induction of ephrin A1 in endothelial cells by TNF-alpha is mediated through both p38 MAPK and SAPK/JNK, but not p42/44 MAPK or NF-kappa B, pathways.

* This work was supported by National Institutes of Health Grant RO1 HD36400 (to J. C.), an American Heart Association grant (to J. C.), grants from Boehringer Ingelheim Pharmaceutical Inc. (to J. C.), National Institutes of Health Training Grant T-32 CA09592 (to N. C.), and core facilities of the Vanderbilt Ingram Cancer Center.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: A-4323, Medical Center North, Vanderbilt University Medical School, Nashville, TN 37232. Tel.: 615-343-3819; Fax: 615-343-7392; E-mail: jin.chen@mcmail.vanderbilt.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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