Retinoids increase human apolipoprotein A-11 expression through activation of the retinoid X receptor but not the retinoic acid receptor
Retinoids increase human apolipoprotein A-11 expression through activation of the retinoid X receptor but not the retinoic acid receptor
复制标题
类视黄醇通过激活类视黄醇 X 受体而非视黄酸受体来增加人载脂蛋白 A-11 表达
DOI:
--
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发表时间:
1996
影响因子:
5.3
通讯作者:
J. Auwerx
中科院分区:
文献类型:
--
作者:
N. Vu;K. Schoonjans;Vladimir Kosykh;Jean Dallongeville;Richard A. Heyman;Bart Staels;J. Auwerx
Considering the link between plasma high-density lipoprotein (HDL) cholesterol levels and a protective effect against coronary artery disease as well as the suggested beneficial effects of retinoids on the production of the major HDL apolipoprotein (apo), apo A-I, the goal of this study was to analyze the influence of retinoids on the expression of apo A-II, the other major HDL protein. Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. In the HepG2 human hepatoblastoma cell line, both at-RA and 9-cis RA as well as the retinoid X receptor (RXR)-specific agonist LGD 1069, but not the RA receptor (RAR) agonist ethyl-p-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)-l-pro penyl]-benzoic acid (TTNPB), induce apo A-II mRNA levels. Transient-transfection experiments with a reporter construct driven by the human apo A-II gene promoter indicated that 9-cis RA and at-RA, as well as the RXR agonists LGD 1069 and LG 100268, induced apo A-II gene expression at the transcriptional level. Only minimal effects of the RAR agonist TTNPB were observed on the apo A-II promoter reporter construct. Unilateral deletions and site-directed mutagenesis identified the J site of the apo A-II promoter mediating the responsiveness to RA. This element contains two imperfect half-sites spaced by 1 oligonucleotide. Cotransfection assays in combination with the use of RXR or RAR agonists showed that RXR but not RAR transactivates the apo A-II promoter through this element. By contrast, RAR inhibits the inductive effects of RXR on the apo A-II J site in a dose-dependent fashion. Gel retardation assays demonstrated that RXR homodimers bind, although with a lower affinity than RAR-RXR heterodimers, to the AH-RXR response element. In conclusion, retinoids induce hepatic apo A-II production at the transcriptional level via the interaction of RXR with an element in the J site containing two imperfect half-sites spaced by 1 oligonucleotide, thereby demonstrating an important role of RXR in controlling human lipoprotein metabolism. Since the J site also confers responsiveness of the apo A-II gene to fibrates and fatty acids via the activation of peroxisome proliferator-activated receptor-RXR heterodimers, this site can be considered a plurimetabolic response element.
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DOI:
10.1016/s0021-9258(19)49613-0
发表时间:
1992-08
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
J. Ladias;M. Hadzopoulou-Cladaras;D. Kardassis;P. Cardot;Jian Cheng;V. Zannis;C. Cladaras;John A. A.
通讯作者:
J. Ladias;M. Hadzopoulou-Cladaras;D. Kardassis;P. Cardot;Jian Cheng;V. Zannis;C. Cladaras;John A. A.
影响因子:
2.9
作者:
Cardot,P;Pastier,D;Lacorte,JM;Mangeney,M;Zannis,VI;Chambaz,J
通讯作者:
Chambaz,J
影响因子:
56.9
作者:
WARDEN, CH;HEDRICK, CC;LUSIS, AJ
通讯作者:
LUSIS, AJ
DOI:
--
发表时间:
1990
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Doolittle,MH;LeBoeuf,RC;Warden,CH;Bee,LM;Lusis,AJ
通讯作者:
Lusis,AJ
DOI:
--
发表时间:
1983
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Lusis,AJ;Taylor,BA;Wangenstein,RW;LeBoeuf,RC
通讯作者:
LeBoeuf,RC