Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells

Atherogenic ω-6 lipids are physiological ligands of peroxisome proliferator-activated receptors (PPARs) and elicit pro- and antiatherogenic responses in vascular cells. The objective of this study was to investigate if ω-6 lipids modulated the early growth response-1 (Egr-1)/PPAR crosstalk thereby a...

Full description

Saved in:
Bibliographic Details
Main Authors: Jia Fei, Carla Cook, Miriah Gillespie, Bangning Yu, Khyra Fullen, Nalini Santanam
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2011/753917
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832565142076784640
author Jia Fei
Carla Cook
Miriah Gillespie
Bangning Yu
Khyra Fullen
Nalini Santanam
author_facet Jia Fei
Carla Cook
Miriah Gillespie
Bangning Yu
Khyra Fullen
Nalini Santanam
author_sort Jia Fei
collection DOAJ
description Atherogenic ω-6 lipids are physiological ligands of peroxisome proliferator-activated receptors (PPARs) and elicit pro- and antiatherogenic responses in vascular cells. The objective of this study was to investigate if ω-6 lipids modulated the early growth response-1 (Egr-1)/PPAR crosstalk thereby altering vascular function. Rat aortic smooth muscle cells (RASMCs) were exposed to ω-6 lipids, linoleic acid (LA), or its oxidized form, 13-HPODE (OxLA) in the presence or absence of a PPARα antagonist (MK886) or PPARγ antagonist (GW9662) or PPAR-specific siRNA. Our results demonstrate that ω-6 lipids, induced Egr-1 and monocyte chemotactic protein-1 (MCP-1) mRNA and protein levels at the acute phase (1–4 hrs) when PPARα was downregulated and at subacute phase (4–12 hrs) by modulating PPARγ, thus resulting in altered monocyte adhesion to RASMCs. We provide novel insights into the mechanism of action of ω-6 lipids on Egr-1/PPAR interactions in vascular cells and their potential in altering vascular function.
format Article
id doaj-art-0d545510e3584b9d9dcf5d691f75000e
institution Kabale University
issn 1687-4757
1687-4765
language English
publishDate 2011-01-01
publisher Wiley
record_format Article
series PPAR Research
spelling doaj-art-0d545510e3584b9d9dcf5d691f75000e2025-02-03T01:09:00ZengWileyPPAR Research1687-47571687-47652011-01-01201110.1155/2011/753917753917Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular CellsJia Fei0Carla Cook1Miriah Gillespie2Bangning Yu3Khyra Fullen4Nalini Santanam5Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Pharmacology and Experimental Therapeutics, LSU Health Sciences Center, New Orleans, LA, USADepartment of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USAAtherogenic ω-6 lipids are physiological ligands of peroxisome proliferator-activated receptors (PPARs) and elicit pro- and antiatherogenic responses in vascular cells. The objective of this study was to investigate if ω-6 lipids modulated the early growth response-1 (Egr-1)/PPAR crosstalk thereby altering vascular function. Rat aortic smooth muscle cells (RASMCs) were exposed to ω-6 lipids, linoleic acid (LA), or its oxidized form, 13-HPODE (OxLA) in the presence or absence of a PPARα antagonist (MK886) or PPARγ antagonist (GW9662) or PPAR-specific siRNA. Our results demonstrate that ω-6 lipids, induced Egr-1 and monocyte chemotactic protein-1 (MCP-1) mRNA and protein levels at the acute phase (1–4 hrs) when PPARα was downregulated and at subacute phase (4–12 hrs) by modulating PPARγ, thus resulting in altered monocyte adhesion to RASMCs. We provide novel insights into the mechanism of action of ω-6 lipids on Egr-1/PPAR interactions in vascular cells and their potential in altering vascular function.http://dx.doi.org/10.1155/2011/753917
spellingShingle Jia Fei
Carla Cook
Miriah Gillespie
Bangning Yu
Khyra Fullen
Nalini Santanam
Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
PPAR Research
title Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
title_full Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
title_fullStr Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
title_full_unstemmed Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
title_short Atherogenic ω-6 Lipids Modulate PPAR- EGR-1 Crosstalk in Vascular Cells
title_sort atherogenic ω 6 lipids modulate ppar egr 1 crosstalk in vascular cells
url http://dx.doi.org/10.1155/2011/753917
work_keys_str_mv AT jiafei atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells
AT carlacook atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells
AT miriahgillespie atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells
AT bangningyu atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells
AT khyrafullen atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells
AT nalinisantanam atherogenicō6lipidsmodulatepparegr1crosstalkinvascularcells