Maresin 1 attenuates pro-inflammatory reactions and ER stress in HUVECs via PPARα-mediated pathway

The current study was designed to investigate the therapeutic effects of Maresin 1 (MAR1) on atherosclerotic response. Human monocytes THP-1 and human umbilical vein endothelial cells (HUVECs) were used to investigate the effects of MAR1 on lipopolysaccharide (LPS)-induced inflammation and apoptosis...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2018-11, Vol.448 (1-2), p.335-347
Main Authors: Jung, Tae Woo, Park, Hyung Sub, Choi, Geum Hee, Kim, Daehwan, Ahn, Sung Ho, Kim, Dong-Seok, Lee, Taeseung, Jeong, Ji Hoon
Format: Article
Language:English
Subjects:
Adhesion
Apoptosis
Arteriosclerosis
Atherosclerosis
Biochemistry
Biomedical and Life Sciences
Cardiology
Cell adhesion molecules
Cytokines
Endoplasmic reticulum
Endothelial cells
Endothelium
Human behavior
Inflammation
Life Sciences
Lipopolysaccharides
Medical Biochemistry
Molecular chains
Monocytes
NF-κB protein
Nuclear reactions
Oncology
Phosphorylation
Proteins
Ribonucleic acid
RNA
siRNA
Stresses
Umbilical vein
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Summary:The current study was designed to investigate the therapeutic effects of Maresin 1 (MAR1) on atherosclerotic response. Human monocytes THP-1 and human umbilical vein endothelial cells (HUVECs) were used to investigate the effects of MAR1 on lipopolysaccharide (LPS)-induced inflammation and apoptosis. In this study, we found that MAR1 induces peroxisome proliferator-activated receptor alpha (PPARα) expression. We also demonstrated that MAR1 suppresses atherosclerotic reactions caused by LPS treatment via a PPARα-dependent pathway. MAR1 treatment inhibited LPS-induced phosphorylation of nuclear factor kappa B (NF-κB) and secretion of pro-inflammatory cytokines in HUVECs and THP-1 cells. In HUVEC cells, expression of adhesion molecules and LPS-stimulated adhesion of THP-1 cells to the endothelium were significantly decreased after MAR1 treatment. Furthermore, LPS-induced endoplasmic reticulum (ER) stress and cell apoptosis was significantly decreased after MAR1 treatment of HUVECs. MAR1 also led to a dose-dependent increase in oxygen-regulated protein 150 (ORP150) expression which is responsible for the inhibition of ER stress. Notably, all of the pro-atherosclerotic effects were completely abrogated by treatment with small interfering (si) RNA targeting PPARα. In conclusion, MAR1 ameliorates LPS-induced atherosclerotic reactions via PPARα-mediated suppression of inflammation and ER stress. Graphical abstract
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-018-3392-y