Cloning of cDNAs Encoding G Protein-Coupled Receptor Expressed in Human Endothelial Cells Exposed to Fluid Shear Stress

1997 ◽  
Vol 240 (3) ◽  
pp. 737-741 ◽  
Author(s):  
Yoshio Takada ◽  
Chihiro Kato ◽  
Shuhei Kondo ◽  
Risa Korenaga ◽  
Joji Ando
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
G Protein ◽  
Fluid Shear Stress ◽  
Human Endothelial Cells ◽  
Fluid Shear ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

Fluid Shear Stress Increases the Expression of Thrombomodulin by Cultured Human Endothelial Cells

1994 ◽  
Vol 205 (2) ◽  
pp. 1345-1352 ◽  
Author(s):  
Y. Takada ◽  
F. Shinkai ◽  
S. Kondo ◽  
S. Yamamoto ◽  
H. Tsuboi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Human Endothelial Cells ◽  
Fluid Shear

scholarly journals Fluid Shear Stress Activates Ca 2+ Influx Into Human Endothelial Cells via P2X4 Purinoceptors

2000 ◽  
Vol 87 (5) ◽  
pp. 385-391 ◽  
Author(s):  
Kimiko Yamamoto ◽  
Risa Korenaga ◽  
Akira Kamiya ◽  
Joji Ando
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Human Endothelial Cells ◽  
Fluid Shear

scholarly journals Shear stress induces Gαq/11 activation independently of G protein-coupled receptor activation in endothelial cells

2017 ◽  
Vol 312 (4) ◽  
pp. C428-C437 ◽  
Author(s):  
Nathaniel G. dela Paz ◽  
Benoît Melchior ◽  
John A. Frangos
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
G Protein ◽  
Molecular Mechanisms ◽  
Fluid Shear Stress ◽  
Receptor Activation ◽  
Proximity Ligation Assay ◽  
Human Coronary Artery ◽  
Gpcr Activation ◽  
G Protein Coupled

Mechanochemical signal transduction occurs when mechanical forces, such as fluid shear stress, are converted into biochemical responses within the cell. The molecular mechanisms by which endothelial cells (ECs) sense/transduce shear stress into biological signals, including the nature of the mechanosensor, are still unclear. G proteins and G protein-coupled receptors (GPCRs) have been postulated independently to mediate mechanotransduction. In this study, we used in situ proximity ligation assay (PLA) to investigate the role of a specific GPCR/Gαq/11 pair in EC shear stress-induced mechanotransduction. We demonstrated that sphingosine 1-phosphate (S1P) stimulation causes a rapid dissociation at 0.5 min of Gαq/11 from its receptor S1P3, followed by an increased association within 2 min of GPCR kinase-2 (GRK2) and β-arrestin-1/2 with S1P3 in human coronary artery ECs, which are consistent with GPCR/Gαq/11 activation and receptor desensitization/internalization. The G protein activator AlF4 resulted in increased dissociation of Gαq/11 from S1P3, but no increase in association between S1P3 and either GRK2 or β-arrestin-1/2. The G protein inhibitor guanosine 5′-(β-thio) diphosphate (GDP-β-S) and the S1P3 antagonist VPC23019 both prevented S1P-induced activation. Shear stress also caused the rapid activation within 7 s of S1P3/Gαq/11. There were no increased associations between S1P3 and GRK2 or S1P3 and β-arrestin-1/2 until 5 min. GDP-β-S, but not VPC23019, prevented dissociation of Gαq/11 from S1P3 in response to shear stress. Shear stress did not induce rapid dephosphorylation of β-arrestin-1 or rapid internalization of S1P3, indicating no GPCR activation. These findings suggest that Gαq/11 participates in the sensing/transducing of shear stress independently of GPCR activation in ECs.

G protein-coupled receptors serve as mechanosensors for fluid shear stress in neutrophils

2006 ◽  
Vol 290 (6) ◽  
pp. C1633-C1639 ◽  
Author(s):  
Ayako Makino ◽  
Eric R. Prossnitz ◽  
Moritz Bünemann ◽  
Ji Ming Wang ◽  
Weijuan Yao ◽  
...  
Keyword(s):  
Shear Stress ◽  
G Protein ◽  
Fluid Shear Stress ◽  
G Protein Coupled Receptors ◽  
Membrane Receptors ◽  
Specific Response ◽  
Constitutive Activity ◽  
Fluid Shear ◽  
Hl60 Cells ◽  
G Protein Coupled

Many cells respond to fluid shear stress but in a cell type-specific fashion. Fluid shear stress applied to leukocytes serves to control pseudopod formation, migration, and other functions. Specifically, fresh neutrophils or neutrophilic leukocytes derived from differentiated HL60 cells respond to fluid shear stress by cytoplasmic pseudopod retraction. The membrane elements that sense fluid shear and induce such a specific response are still unknown, however. We hypothesized that membrane receptors may serve as fluid shear sensors. We found that fluid shear decreased the constitutive activity of G protein-coupled receptors (GPCRs). Inhibition of GPCR constitutive activity by inverse agonists abolished fluid shear stress-induced cell area reduction. Among the GPCRs in neutrophils, the formyl peptide receptor (FPR) exhibits relatively high constitutive activity. Undifferentiated HL60 cells that lacked FPR formed few pseudopods and showed no detectable response to fluid shear stress, whereas expression of FPR in undifferentiated HL60 cells caused pseudopod projection and robust pseudopod retraction during fluid shear. FPR small interfering RNA-transfected differentiated HL60 cells exhibited no response to fluid shear stress. These results suggest that GPCRs serve as mechanosensors for fluid shear stress in neutrophils by decreasing its constitutive activity and reducing pseudopod projection.

scholarly journals Glycocalyx sialic acids regulate Nrf2-mediated signaling by fluid shear stress in human endothelial cells

Redox Biology ◽  
2021 ◽  
Vol 38 ◽  
pp. 101816
Author(s):  
Paraskevi-Maria Psefteli ◽  
Phoebe Kitscha ◽  
Gema Vizcay ◽  
Roland Fleck ◽  
Sarah J. Chapple ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Sialic Acids ◽  
Human Endothelial Cells ◽  
Fluid Shear
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