scholarly journals Oxidized low-density lipoprotein stimulates epithelial sodium channels in endothelial cells of mouse thoracic aorta

2017 ◽  
Vol 175 (8) ◽  
pp. 1318-1328 ◽  
Author(s):  
Chen Liang ◽  
Qiu-Shi Wang ◽  
Xu Yang ◽  
Na Niu ◽  
Qing-Qing Hu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Thoracic Aorta ◽  
Sodium Channels ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Epithelial Sodium Channels

MicroRNA‐328 ameliorates oxidized low‐density lipoprotein‐induced endothelial cells injury through targeting HMGB1 in atherosclerosis

2018 ◽  
Vol 120 (2) ◽  
pp. 1643-1650 ◽  
Author(s):  
Chun‐Yang Wu ◽  
Zhao‐Feng Zhou ◽  
Bin Wang ◽  
Zun‐Ping Ke ◽  
Zhong‐Chun Ge ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

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.

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