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Lipopolysaccharide induced LOX-1 expression via TLR4/MyD88/ROS activated p38MAPK-NF-κB pathway
Zhao W.; Ma G.; Chen X.
2014
Source PublicationVascular Pharmacology
ISSN15371891
Volume63Issue:3Pages:162
Abstract

Lectin-like receptor for oxidized low density lipoprotein (LOX-1) plays a key role in endothelial ox-LDL endocytosis, endothelial dysfunction and atherogenesis. In the present study, the effect of lipopolysaccharide (LPS) on LOX-1 expression and the underlying molecular pathways were investigated. Human umbilical vein endothelial cells (HUVECs) were treated with LPS and the protein expressions of LOX-1, TLR4, TLR2, MyD88, Nox4, Nox2, PI3K, p38MAPK, JNK, ERK, Nrf1, Nrf2 and p65 were examined by Western blotting. The intracellular reactive oxygen species (ROS) production was examined by flow cytometry with fluorescence probe DCFH2-DA. The role of TLR4, MyD88 and Nox4 were determined with specific siRNA. The endothelial ox-LDL uptake and the endothelial-monocyte adhesion were evaluated with DiI-ox-LDL and Hoechst 33342 respectively. The effect of LPS on LOX-1 expression in aorta tissue was also studied with male C57/BL6 mice by intraperitoneal injection of LPS. The results showed that LPS induced LOX-1 protein expression in a time- and concentration-dependent manner. The mRNA expression of LOX-1 was also upregulated. The protein expression of LOX-1 and phosphorylated p38MAPK, p65 was significantly enhanced by LPS both in vitro and in vivo. LPS induced LOX-1 expression was blocked by siRNA for TLR4, MyD88, and Nox4 and inhibitors for p38MAPK, NF-κB, cyclooxygenase-2, and NADPH oxidase. Both LPS induced ox-LDL uptake and endothelial-monocyte adhesion were significantly inhibited by anti-LOX-1 antibody. LPS dramatically induced LOX-1 protein expression in aorta tissues. In conclusion, our data suggested that LPS induces LOX-1 expression via TLR4/MyD88/ROS activated p38MAPK/NF-κB pathway in endothelial cells, which provides new regulatory mechanisms for LOX-1 expression. © 2014 Elsevier Inc.

KeywordEndothelial Cells Lipopolysaccharide Lox-1 Ros
DOIhttp://doi.org/10.1016/j.vph.2014.06.008
URLView the original
Indexed BySCI
Language英语
WOS Research AreaPharmacology & Pharmacy
WOS SubjectPharmacology & Pharmacy
WOS IDWOS:000346218800008
The Source to ArticleScopus
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Cited Times [WOS]:29   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorChen X.
AffiliationState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China
First Author AffilicationInstitute of Chinese Medical Sciences
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Zhao W.,Ma G.,Chen X.. Lipopolysaccharide induced LOX-1 expression via TLR4/MyD88/ROS activated p38MAPK-NF-κB pathway[J]. Vascular Pharmacology,2014,63(3):162.
APA Zhao W.,Ma G.,&Chen X..(2014).Lipopolysaccharide induced LOX-1 expression via TLR4/MyD88/ROS activated p38MAPK-NF-κB pathway.Vascular Pharmacology,63(3),162.
MLA Zhao W.,et al."Lipopolysaccharide induced LOX-1 expression via TLR4/MyD88/ROS activated p38MAPK-NF-κB pathway".Vascular Pharmacology 63.3(2014):162.
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