You need JavaScript to view this

Identification of the human ApoAV gene as a novel ROR{alpha} target gene

Abstract

Retinoic acid receptor-related orphan receptor-{alpha} (ROR{alpha}) (NR1F1) is an orphan nuclear receptor with a potential role in metabolism. Previous studies have shown that ROR{alpha} regulates transcription of the murine Apolipoprotein AI gene and human Apolipoprotein CIII genes. In the present study, we present evidence that ROR{alpha} also induces transcription of the human Apolipoprotein AV gene, a recently identified apolipoprotein associated with triglyceride levels. Adenovirus-mediated overexpression of ROR{alpha} increased the endogenous expression of ApoAV in HepG2 cells and ROR{alpha} also enhanced the activity of an ApoAV promoter construct in transiently transfected HepG2 cells. Deletion and mutation studies identified three AGGTCA motifs in the ApoAV promoter that mediate ROR{alpha} transactivation, one of which overlaps with a previously identified binding site for PPAR{alpha}. Together, these results suggest a novel mechanism whereby ROR{alpha} modulates lipid metabolism and implies ROR{alpha} as a potential target for the treatment of dyslipidemia and atherosclerosis.
Authors:
Lind, Ulrika; [1]  Nilsson, Tina; [1]  McPheat, Jane; [1]  Stroemstedt, Per-Erik; [1]  Bamberg, Krister; [1]  Balendran, Clare; [1]  Kang, Daiwu [1] 
  1. Department of Molecular Pharmacology, AstraZeneca R and D Moelndal (Sweden)
Publication Date:
Apr 29, 2005
Product Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 330; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2005.02.151; PII: S0006-291X(05)00429-8; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Subject:
60 APPLIED LIFE SCIENCES; ADENOVIRUS; ARTERIOSCLEROSIS; GENE REGULATION; GENES; METABOLISM; PROMOTERS; RECEPTORS; RETINOIC ACID; TRANSCRIPTION; TRIGLYCERIDES
OSTI ID:
20709161
Country of Origin:
United States
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0006-291X; BBRCA9; TRN: US05R4267023502
Submitting Site:
INIS
Size:
page(s) 233-241
Announcement Date:
May 01, 2006

Citation Formats

Lind, Ulrika, Nilsson, Tina, McPheat, Jane, Stroemstedt, Per-Erik, Bamberg, Krister, Balendran, Clare, and Kang, Daiwu. Identification of the human ApoAV gene as a novel ROR{alpha} target gene. United States: N. p., 2005. Web. doi:10.1016/j.bbrc.2005.02.151.
Lind, Ulrika, Nilsson, Tina, McPheat, Jane, Stroemstedt, Per-Erik, Bamberg, Krister, Balendran, Clare, & Kang, Daiwu. Identification of the human ApoAV gene as a novel ROR{alpha} target gene. United States. https://doi.org/10.1016/j.bbrc.2005.02.151
Lind, Ulrika, Nilsson, Tina, McPheat, Jane, Stroemstedt, Per-Erik, Bamberg, Krister, Balendran, Clare, and Kang, Daiwu. 2005. "Identification of the human ApoAV gene as a novel ROR{alpha} target gene." United States. https://doi.org/10.1016/j.bbrc.2005.02.151.
@misc{etde_20709161,
title = {Identification of the human ApoAV gene as a novel ROR{alpha} target gene}
author = {Lind, Ulrika, Nilsson, Tina, McPheat, Jane, Stroemstedt, Per-Erik, Bamberg, Krister, Balendran, Clare, and Kang, Daiwu}
abstractNote = {Retinoic acid receptor-related orphan receptor-{alpha} (ROR{alpha}) (NR1F1) is an orphan nuclear receptor with a potential role in metabolism. Previous studies have shown that ROR{alpha} regulates transcription of the murine Apolipoprotein AI gene and human Apolipoprotein CIII genes. In the present study, we present evidence that ROR{alpha} also induces transcription of the human Apolipoprotein AV gene, a recently identified apolipoprotein associated with triglyceride levels. Adenovirus-mediated overexpression of ROR{alpha} increased the endogenous expression of ApoAV in HepG2 cells and ROR{alpha} also enhanced the activity of an ApoAV promoter construct in transiently transfected HepG2 cells. Deletion and mutation studies identified three AGGTCA motifs in the ApoAV promoter that mediate ROR{alpha} transactivation, one of which overlaps with a previously identified binding site for PPAR{alpha}. Together, these results suggest a novel mechanism whereby ROR{alpha} modulates lipid metabolism and implies ROR{alpha} as a potential target for the treatment of dyslipidemia and atherosclerosis.}
doi = {10.1016/j.bbrc.2005.02.151}
journal = []
issue = {1}
volume = {330}
place = {United States}
year = {2005}
month = {Apr}
}