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Originally published In Press as doi:10.1074/jbc.M003464200 on August 31, 2000

J. Biol. Chem., Vol. 275, Issue 52, 41035-41048, December 29, 2000
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Tumor Necrosis Factor-alpha -mediated Protein Kinases in Regulation of Scavenger Receptor and Foam Cell Formation on Macrophage*

Hsien-Yeh HsuDagger § and Yuh-Ching Twu

From the Dagger  Faculty of Medical Technology, Institute of Biotechnology in Medicine, National Yang-Ming University, 112 Taipei and  Transfusion Medicine Laboratory, Department of Medical Research, Mackay Memorial Hospital, 251 Taipei, Taiwan

We previously reported tumor necrosis factor-alpha (TNF) modulates transcriptional and post-transcriptional down-regulation of macrophage scavenger receptor (MSR) (Hsu, H. Y., Nicholson, A. C., and Hajjar, D. P. (1996) J. Biol. Chem. 271, 7767-7773); however, TNF-mediated signaling mechanisms are unknown. Here, we demonstrate that ligation of TNF receptor stimulates activity of p21-activated protein kinase (PAK) and mitogen-activated protein kinases (MAPK) as follows: ERK, JNK, and p38 in murine macrophage J774A.1 cells. Upon activation of protein kinases (PK), TNF rapidly increases MSR message and protein; later it markedly reduces MSR expression. Studies using PK inhibitors and dominant negative constructs demonstrate phosphatidylinositol 3-kinase/Rac1/PAK/JNK and phosphatidylinositol 3-kinase/Rac1/PAK/p38 pathways contribute to important roles in the late stage of TNF down-regulation of MSR expression and taking up of OxLDL. Alternatively, the PKC/MEK1/ERK pathway in the early stage plays a significant role in up-regulation of the MSR gene. By using anti-TNF-R1 agonist antibody, we further confirm TNF-R1-mediated MAPK in regulation of MSR. Furthermore, in MSR gene promoter-driven luciferase reporter assays with TNF, PKC activator increases, but antioxidant N-acetylcysteine, PK inhibitors, and dominant negative constructs decrease luciferase activity in MSR gene promoter-transfected cells. Our current results show the first evidence of crucial roles for TNF-mediated MAPK pathways in the transcriptional regulation of MSR gene and increase MSR expression; in contrast, with TNF longer treatment the pathways down-regulate MSR and foam cell formation probably via post-transcriptional process.

* This work was supported by Research Grant NSC 89-2316-B-010-016-M26 (to H.-Y. H.) from the National Science Council, Executive Yuan, Taiwan.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.

§ Awarded by the Medical Research and Advancement Foundation in memory of Dr. Chi-Shuen Tsou. To whom reprint requests and correspondence should be addressed: Institute of Biotechnology in Medicine, National Yang-Ming University, 115 Li-Nong St., Shih-Pai, Taipei, Taiwan. Tel.: 886-2-2826-7252; Fax: 886-2-2826-4092; E-mail: hyhsu@ym.edu.tw.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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