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Originally published In Press as doi:10.1194/jlr.M200415-JLR200 on May 14, 2003 Originally published In Press as doi:10.1194/jlr.M200415-JLR200 on May 1, 2003

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Journal of Lipid Research, Vol. 44, 1315-1321, July 2003
Copyright © 2003 by American Society for Biochemistry and Molecular Biology

LDL immune complexes stimulate LDL receptor expression in U937 histiocytes via extracellular signal-regulated kinase and AP-1

Yuchang Fu1,{dagger}, Yan Huang1,*,{dagger}, Sumita Bandyopadhyay{dagger}, Gabriel Virella§ and Maria F. Lopes-Virella2,*,{dagger}

* Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC 29401
{dagger} Division of Endocrinology, Diabetes and Medical Genetics, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425
§ Department of Immunology and Microbiology, Medical University of South Carolina, Charleston, SC 29425

2 To whom correspondence should be addressed. e-mail: virellam{at}musc.edu

We have previously shown that LDL-containing immune complexes (LDL-ICs) induce up-regulation of LDL receptor (LDLR) expression in human macrophages. The present study further investigated the molecular mechanisms leading to LDLR up-regulation by LDL-ICs as well as the signaling pathways involved. Results showed that treatment of U937 histiocytes with LDL-ICs did not increase the precursors and the cleaved forms of sterol-regulatory element binding proteins (SREBPs) 1a and 2, suggesting that SREBPs may not be involved in LDLR up-regulation by LDL-ICs. Promoter deletion and mutation studies showed that the AP-1 binding sites were essential for LDL-IC-stimulated LDLR expression. Electrophoretic mobility shift assays further demonstrated that LDL-ICs stimulated transcription factor AP-1 activity. Studies assessing the signaling pathways involved in LDLR up-regulation by LDL-ICs showed that the up-regulation of LDLR was extracellular signal-regulated kinase (ERK) dependent.

In conclusion, the present study shows that LDL-ICs up-regulate LDLR expression via the ERK signaling pathway and the AP-1 motif-dependent transcriptional activation.

Supplementary key words low density lipoprotein • mitogen-activated protein kinase • activator protein • macrophages • signal transduction


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