Shear stress contributes to t-PA mRNA expression in human endothelial progenitor cells and nonthrombogenic potential of small diameter artificial vessels

2006 ◽  
Vol 342 (2) ◽  
pp. 577-584 ◽  
Author(s):  
Zhen Yang ◽  
Jun Tao ◽  
Jie-Mei Wang ◽  
Chang Tu ◽  
Ming-Guo Xu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Mrna Expression ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Small Diameter ◽  
Endothelial Progenitor

Shear stress regulates inflammatory and thrombogenic gene transcripts in cultured human endothelial progenitor cells

2010 ◽  
Vol 104 (09) ◽  
pp. 582-591 ◽  
Author(s):  
Trine Lund ◽  
Stig Hermansen ◽  
Thomas Andreasen ◽  
Jan Olsen ◽  
Bjarne Østerud ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Mrna Expression ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mrna Levels ◽  
Endothelial Progenitor ◽  
Gene Transcripts ◽  
Nos Inhibitor

SummaryShear stress has an established effect on mature endothelial cells, but less is known about how shear stress regulates endothelial progenitor cells (EPCs). In vitro expanded EPCs isolated from adult human blood represent a novel tool in regenerative vessel therapy. However, in vitro culturing may generate cells with unfavourable properties. The aim of the present study was therefore to assess whether shear stress may influence the inflammatory and thrombotic phenotype of in vitro expanded EPCs. In late outgrowth EPCs, 6 hours of shear stress (6.0 dynes/ cm2) significantly reduced the mRNA levels of IL-8, COX2, and tissue factor (TF) compared to static controls. This was associated with a reduced TF activity. In contrast, mRNA expression of NOS3 was significantly increased following 6 and 24 hours of shear stress. In accordance with this, NOS3 protein expression was increased following 24 hours of shear stress. Overall stimulation with the proinflammatory mediator, TNFα, for the final 2 hours increased the mRNA expression of IL-6, IL-8, MCP-1, ICAM1, and TF. However exposure to 6 hours of shear stress significantly suppressed the inductory potential of TNFα to increase the mRNA levels of IL-6, IL-8, COX2, and TF. Additionally, TNFα increased TF activity approximately 10 times, an effect that was also significantly reduced by exposure to 6 and 24 hours of shear stress. The effect of shear on the gene levels of TF and NOS3 were not blocked by the NOS inhibitor L-NAME. These observations suggest that EPCs are capable of functionally responding to shear stress.

scholarly journals Shear stress increases Cu/Zn SOD activity and mRNA expression in human endothelial progenitor cells

2007 ◽  
Vol 21 (5) ◽  
pp. 353-358 ◽  
Author(s):  
J Tao ◽  
Z Yang ◽  
J-Mei Wang ◽  
L-Chun Wang ◽  
C-F Luo ◽  
...  
Keyword(s):  
Shear Stress ◽  
Mrna Expression ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Sod Activity

β2AR-dependent signaling contributes to in-vivo reendothelialization capacity of endothelial progenitor cells by shear stress

2020 ◽  
Vol 38 (1) ◽  
pp. 82-94 ◽  
Author(s):  
Qingsong Hu ◽  
Tao Zhang ◽  
Yan Li ◽  
Jianyi Feng ◽  
Ruqiong Nie ◽  
...  
Keyword(s):  
Shear Stress ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor

scholarly journals Vulnerability to shear stress caused by altered peri-endothelial matrix is a key feature of Moyamoya disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Muneaki Matsuo ◽  
Satomi Nadanaka ◽  
Minami Soga ◽  
Taku Sugiyama ◽  
Shota Serigano ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Moyamoya Disease ◽  
Internal Carotid ◽  
Terminal Portion ◽  
Endothelial Progenitor ◽  
Wall Shear ◽  
Thickened Intima

AbstractMoyamoya disease (MMD) is characterized by progressive bilateral stenotic changes in the terminal portion of the internal carotid arteries. Although RNF213 was identified as a susceptibility gene for MMD, the exact pathogenesis remains unknown. Immunohistochemical analysis of autopsy specimens from a patient with MMD revealed marked accumulation of hyaluronan and chondroitin sulfate (CS) in the thickened intima of occlusive lesions of MMD. Hyaluronan synthase 2 was strongly expressed in endothelial progenitor cells in the thickened intima. Furthermore, MMD lesions showed minimal staining for CS and hyaluronan in the endothelium, in contrast to control endothelium showing positive staining for both. Glycosaminoglycans of endothelial cells derived from MMD and control induced pluripotent stem cells demonstrated a decreased amount of CS, especially sulfated CS, in MMD. A computational fluid dynamics model showed highest wall shear stress values in the terminal portion of the internal carotid artery, which is the predisposing region in MMD. Because the peri-endothelial extracellular matrix plays an important role in protection, cell adhesion and migration, an altered peri-endothelial matrix in MMD may contribute to endothelial vulnerability to wall shear stress. Invading endothelial progenitor cells repairing endothelial injury would produce excessive hyaluronan and CS in the intima, and cause vascular stenosis.

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