Actin stress fiber pre-extension in human aortic endothelial cells

2008 ◽  
Vol 65 (4) ◽  
pp. 281-294 ◽  
Author(s):  
Lan Lu ◽  
Yunfeng Feng ◽  
William J. Hucker ◽  
Sara J. Oswald ◽  
Gregory D. Longmore ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Stress Fiber ◽  
Actin Stress Fiber ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals P773Uric acid regulates multiple interacting major cellular pathways in human aortic endothelial cells: a global proteome approach

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S142.1-S142
Author(s):  
A Oberbach ◽  
V Adams ◽  
N Schlichting ◽  
N Jehmich ◽  
U Voelker ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Cellular Pathways ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Sensitization of Human Aortic Endothelial Cells to Lipopolysaccharide via Regulation of Toll-Like Receptor 4 by Bacterial Fimbria-Dependent Invasion

2005 ◽  
Vol 73 (12) ◽  
pp. 8050-8059 ◽  
Author(s):  
Hiromichi Yumoto ◽  
Hsin-Hua Chou ◽  
Yusuke Takahashi ◽  
Michael Davey ◽  
Frank C. Gibson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Periodontal Disease ◽  
Deficient Mutant ◽  
Wild Type ◽  
Microbial Infection ◽  
Monocyte Chemoattractant Protein 1 ◽  
Aortic Endothelial Cells ◽  
E Coli ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

ABSTRACT Toll-like receptors (TLRs) are differentially up-regulated in response to microbial infection and chronic inflammatory diseases such as atherosclerosis. Epidemiological data support the idea that periodontal disease may be a risk factor for acceleration of atherosclerosis. Porphyromonas gingivalis, the etiological agent of periodontal disease, invades endothelium, has been detected in human atheromatous tissue, and accelerates atheroma formation in apolipoprotein E−/− mice with concurrent induction of TLRs in the aorta. As endothelial cells can present antigen via TLRs and play an important role in the development of atherosclerosis, we examined TLR expression in human aortic endothelial cells (HAEC) cultured with wild-type P. gingivalis, a fimbria-deficient mutant, and purified antigens. We observed increased TLR expression in HAEC infected with wild-type P. gingivalis by fluorescence-activated cell sorter, but not with noninvasive, fimbria-deficient mutant or purified P. gingivalis antigens. Following a wild-type P. gingivalis challenge, functional TLR2 and TLR4 activation was assessed by subsequent stimulation with TLR agonists Staphylococcus aureus lipoteichoic acid (SLTA; TLR2 ligand) and Escherichia coli lipopolysaccharide (LPS; TLR4 ligand). Unchallenged HAEC failed to elicit monocyte chemoattractant protein 1 (MCP-1) in response to LPS or SLTA but did so when cultured with wild-type P. gingivalis. P. gingivalis-induced TLR2 and -4 expression on HAEC functionally reacted to SLTA and E. coli LPS as measured by a further increase in MCP-1 production. Furthermore, MCP-1 expression elicited by E. coli LPS was inhibitable with TLR4-specific antibody and polymyxin B. These results indicate that invasive P. gingivalis stimulates TLR expression on the surface of endothelium and these primed cells respond to defined TLR-specific ligands.

scholarly journals Vitamin D3 attenuates doxorubicin-induced senescence of human aortic endothelial cells by upregulation of IL-10 via the pAMPKα/Sirt1/Foxo3a signaling pathway

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252816
Author(s):  
Lei Chen ◽  
Rachel Holder ◽  
Charles Porter ◽  
Zubair Shah
Keyword(s):  
Endothelial Cells ◽  
Vitamin D3 ◽  
Protective Effects ◽  
Cardiovascular Toxicity ◽  
Complex Activity ◽  
Aortic Endothelial Cells ◽  
Cardiovascular Damage ◽  
Cycle Arrest ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

The toxicity of doxorubicin to the cardiovascular system often limits its benefits and widespread use as chemotherapy. The mechanisms involved in doxorubicin-induced cardiovascular damage and possible protective interventions are not well-explored. Using human aortic endothelial cells, we show vitamin D3 strongly attenuates doxorubicin-induced senescence and cell cycle arrest. We further show the protective effects of vitamin D3 are mediated by the upregulation of IL-10 and FOXO3a expression through fine modulation of pAMPKα/SIRT1/FOXO3a complex activity. These results have great significance in finding a target for mitigating doxorubicin-induced cardiovascular toxicity.

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