scholarly journals Studying the Mechanobiology of Aortic Endothelial Cells Under Cyclic Stretch Using a Modular 3D Printed System

2021 ◽  
Vol 9 ◽  
Author(s):  
Sergio Aguilera Suarez ◽  
Nadia Chandra Sekar ◽  
Ngan Nguyen ◽  
Austin Lai ◽  
Peter Thurgood ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Modular Design ◽  
Cyclic Stretch ◽  
Aortic Endothelial Cells ◽  
Cellular Processes ◽  
Driven System ◽  
3D Printed ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Here, we describe a motorized cam-driven system for the cyclic stretch of aortic endothelial cells. Our modular design allows for generating customized spatiotemporal stretch profiles by varying the profile and size of 3D printed cam and follower elements. The system is controllable, compact, inexpensive, and amenable for parallelization and long-term experiments. Experiments using human aortic endothelial cells show significant changes in the cytoskeletal structure and morphology of cells following exposure to 5 and 10% cyclic stretch over 9 and 16 h. The system provides upportunities for exploring the complex molecular and cellular processes governing the response of mechanosensitive cells under cyclic stretch.

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.

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