Induction of CD36 by all-trans retinoic acid: retinoic acid receptor signaling in the pathogenesis of atherosclerosis
(2001) In FASEB Journal 15(7). p.1221-1223- Abstract
- 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 all-trans 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... (More)
- 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 all-trans 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-a and -g in the lesions, which indicates that atRA may contribute to foam cell formation and the progress of atherosclerosis. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1121864
- author
- Wuttge, Dirk LU ; Romert, A ; Eriksson, U ; Torma, H ; Hansson, G K and Sirsjo, A
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- retinoic acid receptor, oxidized low-density lipoprotein, CD36, atherosclerosis, all-trans retinoic acid
- in
- FASEB Journal
- volume
- 15
- issue
- 7
- pages
- 1221 - 1223
- publisher
- Wiley
- external identifiers
-
- pmid:11344094
- scopus:0035347298
- ISSN
- 1530-6860
- DOI
- 10.1096/fj.00-0488fje
- language
- English
- LU publication?
- no
- id
- 7f70d1fb-f564-44d9-926a-64f96c1cfe61 (old id 1121864)
- date added to LUP
- 2016-04-01 17:00:50
- date last changed
- 2023-09-05 05:35:07
@article{7f70d1fb-f564-44d9-926a-64f96c1cfe61,
abstract = {{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 all-trans 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-a and -g in the lesions, which indicates that atRA may contribute to foam cell formation and the progress of atherosclerosis.}},
author = {{Wuttge, Dirk and Romert, A and Eriksson, U and Torma, H and Hansson, G K and Sirsjo, A}},
issn = {{1530-6860}},
keywords = {{retinoic acid receptor; oxidized low-density lipoprotein; CD36; atherosclerosis; all-trans retinoic acid}},
language = {{eng}},
number = {{7}},
pages = {{1221--1223}},
publisher = {{Wiley}},
series = {{FASEB Journal}},
title = {{Induction of CD36 by all-trans retinoic acid: retinoic acid receptor signaling in the pathogenesis of atherosclerosis}},
url = {{http://dx.doi.org/10.1096/fj.00-0488fje}},
doi = {{10.1096/fj.00-0488fje}},
volume = {{15}},
year = {{2001}},
}