Oxidized Low-Density Lipoprotein Stimulates Nitric Oxide Release by Rabbit Aortic Endothelial Cells

1995 ◽  
Vol 207 (1) ◽  
pp. 231-237 ◽  
Author(s):  
D.M. Fries ◽  
R.G. Penha ◽  
E.A. Damico ◽  
D.S.P. Abdalla ◽  
H.P. Monteiro
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Aortic Endothelial Cells ◽  
Nitric Oxide Release ◽  
Aortic Endothelial

LOX-1-dependent transcriptional regulation in response to oxidized LDL treatment of human aortic endothelial cells

2009 ◽  
Vol 296 (6) ◽  
pp. C1329-C1337 ◽  
Author(s):  
Mark D. Mattaliano ◽  
Christine Huard ◽  
Wei Cao ◽  
Andrew A. Hill ◽  
Wenyan Zhong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Human Aortic Endothelial Cell ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Camp Response Element ◽  
Response Element ◽  
Aortic Endothelial

Oxidized low-density lipoprotein (OxLDL) has been implicated as a proatherogenic factor with a pathological role in the induction of endothelial dysfunction. Endothelial cells bind and uptake OxLDL primarily through the scavenger receptor lectin-like oxidized-low-density lipoprotein receptor-1 (LOX-1), which is believed to mediate critical effects of OxLDL in endothelial cells. To examine the biological events following LOX-1 activation by OxLDL, we used cDNA microarray analysis to globally analyze gene expression changes induced by OxLDL treatment of human aortic endothelial cell line (HAECT) cells overexpressing LOX-1. Consistent with reported functions of OxLDL, in control HAECT cells, OxLDL elicited gene changes in the oxidative stress pathway and other signaling pathways related to OxLDL. With OxLDL treatment, LOX-1-dependent gene expression changes associated with inflammation, cell adhesion, and signal transduction were observed. The transcripts of a number of cytokines and chemokines were induced, which included interleukin-8, CXCL2, CXCL3, and colony-stimulating factor-3. The secretion of these cytokines was confirmed by enzyme-linked immunosorbent assay analysis. In addition, our data revealed a novel link between LOX-1 and a number of genes, including Delta/notch-like epidermal growth factor repeat containing, stanniocalcin-1, cAMP response element modulator, and dual specificity phosphatase 1. Promoter analysis on the genes that changed as a result of LOX-1 activation by OxLDL allowed us to identify early growth response 1 and cAMP response element-binding protein as potential novel transcription factors that function downstream of LOX-1. Our study has enabled us to elucidate the gene expression changes following OxLDL activation of LOX-1 in endothelial cells and discover novel downstream targets for LOX-1.

Puerarin protects endothelial cells from oxidized low density lipoprotein induced injuries via the suppression of LOX-1 and induction of eNOS

2014 ◽  
Vol 92 (4) ◽  
pp. 299-306 ◽  
Author(s):  
Mei-hua Bao ◽  
Yi-wen Zhang ◽  
Xiao-ya Lou ◽  
Yan Xiao ◽  
Yu Cheng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Cell Viability ◽  
Nuclear Translocation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
No Production ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Cox 2

Oxidized low density lipoprotein (oxLDL) induced injury of endothelial cells is considered to be the first step in the pathogenesis of atherosclerosis. This study aimed to investigate some of the effects and mechanisms of puerarin on oxLDL-induced endothelial injuries. We measured cell viability, and the release of lactate dehydrogenase (LDH), nitric oxide (NO), and interleukin-8 (IL-8) to evaluate the protective effects of puerarin. Intracellular reactive oxygen species (ROS) were detected using 2′,7′-dichlorofluorescein diacetate (DCFH-DA). The expression of lectin-like low-density lipoprotein receptor-1 (LOX-1), endothelial nitric oxide synthase (eNOS), cyclooxygenase 2 (COX-2), p38MAPK, and protein kinase B (PKB) phosphorylation, nuclear factor-κB (NF-κB) nuclear translocation, and inhibitor of κB (IκB) degradation were detected using quantitative real-time PCR or Western blot. The results showed that oxLDL significantly decreased cell viability, increased LDH and IL-8 release, inhibited NO production, and induced COX-2 expression. Pretreatment with puerarin led to a strong inhibition of these effects. OxLDL stimulated the expression of LOX-1, the overproduction of ROS, the phosphorylation of p38MAPK, the dephosphorylation of PKB, activation of NF-κB, and the degradation of IκB. These oxLDL-induced effects were suppressed after puerarin pretreatment. These results suggest that puerarin inhibits oxLDL-induced endothelial cell injuries, at least in part, via inhibition of the LOX-1-mediated p38MAPK–NF-κB inflammatory and the PKB–eNOS signaling pathways.

β-Sitosterol regulated microRNAs in endothelial cells against an oxidized low-density lipoprotein

2020 ◽  
Vol 11 (2) ◽  
pp. 1881-1890 ◽  
Author(s):  
Yue-Hua Jiang ◽  
Xiao Li ◽  
Weipin Niu ◽  
DongLi Wang ◽  
Bo Wu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Mitochondrial Function ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Protective Effects ◽  
Oxidized Low Density Lipoprotein ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells

β-sitosterol is shown to demonstrate endothelial protective effects, which inhibited apoptosis, increased cell migration, and improved mitochondrial function of human aortic endothelial cells.

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