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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:825.)
© 2001 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Identification of a -Interferon–Responsive Element in the Promoter of the Human Macrophage Scavenger Receptor A Gene

Thomas Grewal; Elena Priceputu; Jean Davignon; Lise Bernier

From the Hyperlipidemia and Atherosclerosis Research Group, Clinical Research Institute of Montreal, Montreal, Quebec, Canada. Thomas Grewal is currently at the Universität Hamburg, Universitätskrankenhaus Eppendorf, Medizinische Klinik, Hamburg, Germany.

Correspondence to Dr Lise Bernier, Hyperlipidemia and Atherosclerosis Research Group, Clinical Research Institute of Montreal, 110 Pine Ave W, Montreal, Quebec H2W 1R7, Canada. E-mail berniel{at}ircm.qc.ca

Abstract—In the present study, we demonstrate -interferon (-IFN)–inducible scavenger receptor A (SR-A) mRNA expression during the early stages of THP-1 and blood monocyte differentiation. Predominant induction of SR-A type II mRNA parallels the increased accumulation of cholesteryl esters under these conditions. A potential signal transducer and activator of transcription (STAT1) binding site (-interferon activation site) in the SR-A promoter demonstrates -IFN–inducible DNA binding activity and is most likely responsible for the -IFN–dependent expression of an SR-A promoter–luciferase fusion construct. In contrast, -IFN inhibits SR-A expression in mature macrophages as well as after prolonged -IFN incubation of THP-1 monocytes. Taken together, these results demonstrate opposite effects of -IFN on SR-A expression and activity during the early versus late stages of monocyte maturation. -IFN–induced STAT1 activation, leading to increased SR-A expression, could therefore play an important role in the initial steps of foam cell formation and xanthomatosis.

Key Words: scavenger receptor type A • -interferon • STAT1 • GAS element • macrophage activation

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