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Induction of CD36 by all-trans retionic acid: retinoic acid receptor signaling in the pathogenesis of atherosclerosis
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. (Dermatology and Venereology)
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2001 (English)In: The FASEB Journal, ISSN 0892-6638, Vol. 15, no 7, 1221-3 p.Article in journal (Refereed) Published
Abstract [en]

Scavenger receptors mediating the uptake of oxidized low-density lipoproteins (oxLDL) by macrophages play a crucial role in foam cell formation during atherosclerosis. One member of this receptor family, the thrombospondin receptor CD36, has recently been shown to mediate a major part of the oxLDL-induced aggravation of atherosclerotic lesions. Here, we show that the expression of CD36 protein and mRNA in human monocytic THP-1 cells is increased by alltrans retinoic acid (atRA), a derivative of the essential Vitamin A, which leads to increased uptake of oxLDL. CD3106, a specific antagonist at the retinoic acid receptor (RAR), inhibited the atRA-induced CD36 expression, whereas the RAR-specific agonist CD367 induced CD36 to the same degree as atRA. This indicates an RAR-mediated CD36 induction. AtRA and oxLDL had synergistic effects in up-regulating CD36 when in both THP-1 cells and primary monocytes. Applying a sensitive RAR-GAL-4 reporter assay, we could demonstrate RAR ligands in human atherosclerotic lesions. In addition, immunohistochemistry showed RAR- which indicates that atRA may contribute to foam cell formation and the progress of atherosclerosis.

Place, publisher, year, edition, pages
2001. Vol. 15, no 7, 1221-3 p.
Keyword [en]
CD36, atherosclerosis, oxidized low-density lipoprotein, retinoic acid receptor, all-trans retinoic acid
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-54933DOI: 10.1096/fj.00-0488fje.PubMedID: 11344094OAI: oai:DiVA.org:uu-54933DiVA: diva2:82842
Available from: 2008-10-17 Created: 2008-10-17 Last updated: 2009-10-14Bibliographically approved

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