Collective Influence of Substrate Chemistry with Physiological Fluid Shear Stress on Human Umbilical Vein Endothelial Cells

Author(s):  
Yan Li ◽  
Zhongjie Qin ◽  
Lin Zhou ◽  
Khawar Ali Shahzad ◽  
Delin Xia
2012 ◽  
Vol 7 (1) ◽  
pp. 110-114 ◽  
Author(s):  
LIANG-LIANG SUN ◽  
LE ZHANG ◽  
XIANG-LAN MENG ◽  
FENG ZHANG ◽  
YUN ZHAO ◽  
...  

2013 ◽  
Vol 74 ◽  
pp. 36-40 ◽  
Author(s):  
Feng Zhang ◽  
Le Zhang ◽  
Liang-liang Sun ◽  
Xiang-lan Meng ◽  
Yun Zhao ◽  
...  

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Nicolas Baeyens ◽  
Stefania Nicoli ◽  
Brian G Coon ◽  
Tyler D Ross ◽  
Koen Van den Dries ◽  
...  

Vascular remodeling under conditions of growth or exercise, or during recovery from arterial restriction or blockage is essential for health, but mechanisms are poorly understood. It has been proposed that endothelial cells have a preferred level of fluid shear stress, or ‘set point’, that determines remodeling. We show that human umbilical vein endothelial cells respond optimally within a range of fluid shear stress that approximate physiological shear. Lymphatic endothelial cells, which experience much lower flow in vivo, show similar effects but at lower value of shear stress. VEGFR3 levels, a component of a junctional mechanosensory complex, mediate these differences. Experiments in mice and zebrafish demonstrate that changing levels of VEGFR3/Flt4 modulates aortic lumen diameter consistent with flow-dependent remodeling. These data provide direct evidence for a fluid shear stress set point, identify a mechanism for varying the set point, and demonstrate its relevance to vessel remodeling in vivo.


1996 ◽  
Vol 271 (3) ◽  
pp. C994-C1000 ◽  
Author(s):  
S. Li ◽  
R. S. Piotrowicz ◽  
E. G. Levin ◽  
Y. J. Shyy ◽  
S. Chien

The small molecular mass heat shock protein of 27 kDa (HSP27) has been shown to influence actin filament dynamics and endothelial cell behavior in ways similar to those observed during laminar flow. We have employed human umbilical vein endothelial cells to determine whether fluid shear stress affects HSP27 expression or phosphorylation. After a shear stress of 16 dyn/cm2, HSP27 became more highly phosphorylated, with maximum increase in phosphorylation levels (3-fold) attained by 30 min and sustained for at least 20 h. HSP27 antigen levels did not change; however, HSP27 mRNA levels decreased by 20% after 16 h. In bovine aortic endothelial cells stably transfected with the wild-type human HSP27 gene, shear stress induced the phosphorylation of both the exogenous human HSP27 and the endogenous bovine HSP25. The product of a transfected mutant HSP27 gene in which the putative phosphorylation sites Ser-15, Ser-78, and Ser-82 had been replaced with Gly was not phosphorylated. Thus the modulation of HSP27 and its activity by shear stress is mediated through a posttranslational mechanism and differs from the shear stress induction of immediate early genes at the level of transcription.


2001 ◽  
Vol 280 (5) ◽  
pp. H2214-H2221 ◽  
Author(s):  
Risa Korenaga ◽  
Kimiko Yamamoto ◽  
Norihiko Ohura ◽  
Takaaki Sokabe ◽  
Akira Kamiya ◽  
...  

Endothelial purinoceptors play an important role in vascular responses to extracellular adenine nucleotides and hemodynamic forces. Here we report that P2X4 purinoceptor expression in human umbilical vein endothelial cells is transcriptionally downregulated by fluid shear stress. When human umbilical vein endothelial cells were subjected to a laminar shear stress of 15 dyn/cm2, P2X4 mRNA levels began to decrease within 1 h and further decreased with time, reaching 60% at 24 h. Functional analysis of the 1.9-kb P2X4 5′-promoter indicated that a 131-bp segment (−112 to +19 bp relative to the transcription start site) containing a consensus binding site for the Sp1 transcription factor was critical for the shear stress responsiveness. Mutations of the Sp1 site decreased the basal level of transcription and abolished the response of the P2X4 promoter to shear stress. Electrophoretic mobility shift assays showed a marked decrease in binding of Sp1 to the Sp1 consensus element in shear-stressed cells, suggesting that Sp1 mediates the shear stress-induced downregulation of P2X4 gene transcription.


Author(s):  
Hojin Kang ◽  
Kayla J. Bayless ◽  
Roland Kaunas

We have previously developed a cell culture model to study the effects of angiogenic factors, such as sphingosine-1-phosphate (S1P), on the invasion of endothelial cells into the underlying extracellular matrix. In addition to biochemical stimuli, vascular endothelial cells are subjected to fluid shear stress due to blood flow. The present study is aimed at determining the effects of fluid shear stress on endothelial cell invasion into collagen gels. A device was constructed to apply well-defined fluid shear stresses to confluent human umbilical vein endothelial cells (HUVECs) seeded on collagen gels. Fluid shear stress induced significant increases in cell invasion with a maximal induction at ∼5 dyn/cm2. These results provide evidence that fluid shear stress is a significant stimulus for endothelial cell invasion and may play a role in regulating angiogenesis.


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