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.

Low-density lipoprotein from active SLE patients is more atherogenic to endothelial cells than low-density lipoprotein from the same patients during remission

Rheumatology ◽  
2020 ◽  
Author(s):  
Ricardo Rodríguez-Calvo ◽  
Montse Guardiola ◽  
Iris Oliva ◽  
Hugo Arrando ◽  
Idoia Arranz ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Aortic Endothelial Cells ◽  
Ldl Particles ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Abstract Objectives SLE patients have an enhanced risk of atherosclerosis and cardiovascular disease. However, the increased prevalence of cardiovascular disease is not fully explained by traditional Framingham cardiovascular risk factors. Specific features of low-density lipoprotein (LDL) particles, other than plasma concentration, may induce accelerated atherosclerosis at early stages in these patients. Thus, we aimed to explore the impact of LDL from both active and inactive SLE patients on human aortic endothelial cells. Methods Human aortic endothelial cells were stimulated with the same concentration of LDL particles isolated from pooled serum that was collected from 13 SLE patients during both active and inactive states. Gene expression and cell migration assays were performed. Results Circulating LDL particles obtained from healthy volunteers and SLE patients in both remission and flare states were comparable in terms of number, cholesterol and triglyceride content, and net electric charge. Stimulation of cells with LDL from active SLE patients induced the expression of vascular cell adhesion molecule 1 (∼2.0-fold, P < 0.05), monocyte chemoattractant protein 1 (∼2.0-fold, P < 0.05) and matrix metallopeptidase 2 (∼1.6-fold, P < 0.01) compared with cells stimulated with LDL from inactive SLE patients. Additionally, LDL extracted from active patients increased cell migration in a wound-healing assay (1.4-fold, P < 0.05). Conclusion Our data show that, at the same LDL concentration, LDL from active SLE patients had increased proatherogenic effects on endothelial cells compared with LDL from the same patients when in an inactive or remission state.

Diphenyl diselenide protects endothelial cells against oxidized low density lipoprotein-induced injury: Involvement of mitochondrial function

Biochimie ◽  
2014 ◽  
Vol 105 ◽  
pp. 172-181 ◽  
Author(s):  
Mariana Appel Hort ◽  
Marcos Raniel Straliotto ◽  
Jade de Oliveira ◽  
Nívea Dias Amoêdo ◽  
João Batista Teixeira da Rocha ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mitochondrial Function ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Diphenyl Diselenide ◽  
Oxidized Low Density Lipoprotein

scholarly journals Lectin-like oxidized low-density lipoprotein receptor 1 mediates phagocytosis of aged/apoptotic cells in endothelial cells

1998 ◽  
Vol 95 (16) ◽  
pp. 9535-9540 ◽  
Author(s):  
Kozo Oka ◽  
Tatsuya Sawamura ◽  
Ken-ichiro Kikuta ◽  
Shigekazu Itokawa ◽  
Noriaki Kume ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Chinese Hamster ◽  
Density Lipoprotein ◽  
Low Density ◽  
Apoptotic Cells ◽  
Wild Type ◽  
Oxidized Low Density Lipoprotein ◽  
Aortic Endothelial Cells ◽  
Density Lipoprotein Receptor

Recognition of the exposure of phosphatidylserine (PS) on the outer surface of plasma membrane has been implicated in the phagocytosis of aged/apoptotic cells. Because oxidized low-density lipoprotein (OxLDL) has been reported to block the phagocytosis, here we examined whether lectin-like OxLDL receptor 1 (LOX-1), the OxLDL receptor in endothelial cells, mediates phagocytosis of aged/apoptotic cells by endothelial cells. Cultured bovine aortic endothelial cells (BAE) and Chinese hamster ovary (CHO) cells expressing bovine LOX-1 (BLOX-1-CHO), but not wild-type CHO-K1 cells, bound aged red blood cells (RBC) and apoptotic cells, which were further phagocytosed. The binding of aged RBC and the phagocytosis of apoptotic cells were inhibited by OxLDL, acetyl LDL, and other LOX-1 ligands in both BAE and BLOX-1-CHO. mAb against LOX-1 blocked the binding of aged RBC to BAE, suggesting a role for LOX-1 in the recognition of aged cells. The recombinant soluble LOX-1 inhibited the interactions of aged/apoptotic cells with both BLOX-1-CHO and BAE and distinguished aged RBC from native RBC and apoptotic cells from native cells. PS liposome inhibited these LOX-1-mediated interactions with aged/apoptotic cells, suggesting LOX-1 recognizes PS of the apoptotic cells. PS exposed on the surface of apoptotic cells is known to be procoagulant. Accordingly, increased OxLDL may be one of the reasons for enhanced coagulation in atherosclerosis, inhibiting the removal of apoptotic cells.

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