Role of the Glycocalyx in Fluid Shear Stress Modulation of Heme Oxygenase-1 in Human Endothelial Cells

2016 ◽  
Vol 100 ◽  
pp. S148
Author(s):  
Paraskevi-Maria Psefteli ◽  
Mark Fowler ◽  
Richard Draijer ◽  
Giovanni E. Mann ◽  
Richard Siow
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Heme Oxygenase ◽  
Fluid Shear Stress ◽  
Heme Oxygenase 1 ◽  
Human Endothelial Cells ◽  
Fluid Shear

Role of cadherins and plakoglobin in interendothelial adhesion under resting conditions and shear stress

1997 ◽  
Vol 273 (5) ◽  
pp. H2396-H2405 ◽  
Author(s):  
Hans-Joachim Schnittler ◽  
Bernd Püschel ◽  
Detlev Drenckhahn
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Time Course ◽  
Fluid Shear Stress ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Platelet Endothelial Cell Adhesion ◽  
Cell Adhesion Molecule 1 ◽  
Arterial Endothelial Cells

The role of cadherins and the cadherin-binding cytosolic protein plakoglobin in intercellular adhesion was studied in cultured human umbilical venous endothelial cells exposed to fluid shear stress. Extracellular Ca2+depletion (<10−7 M) caused the disappearance of both cadherins and plakoglobin from junctions, whereas the distribution of platelet endothelial cell adhesion molecule 1 (PECAM-1) remained unchanged. Cells stayed fully attached to each other for several hours in low Ca2+ but began to dissociate under flow conditions. At the time of recalcification, vascular endothelial (VE) cadherin and β-catenin became first visible at junctions, followed by plakoglobin with a delay of ∼20 min. Full fluid shear stress stability of the junctions correlated with the time course of the reappearance of plakoglobin. Inhibition of plakoglobin expression by microinjection of antisense oligonucleotides did not interfere with the junctional association of VE-cadherin, PECAM-1, and β-catenin. The plakoglobin-deficient cells remained fully attached to each other under resting conditions but began to dissociate in response to flow. Shear stress-induced junctional dissociation was also observed in cultures of plakoglobin-depleted arterial endothelial cells of the porcine pulmonary trunk. These observations show that interendothelial adhesion under hydrodynamic but not resting conditions requires the junctional location of cadherins associated with plakoglobin. β-Catenin cannot functionally compensate for the junctional loss of plakoglobin, and PECAM-1-mediated adhesion is not sufficient for monolayer integrity under flow.

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

Cytoprotection of human endothelial cells from menadione cytotoxicity by caffeic acid phenethyl ester: The role of heme oxygenase-1

2008 ◽  
Vol 591 (1-3) ◽  
pp. 28-35 ◽  
Author(s):  
Xinyu Wang ◽  
Salomon Stavchansky ◽  
Baiteng Zhao ◽  
James A. Bynum ◽  
Sean M. Kerwin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Caffeic Acid ◽  
Heme Oxygenase ◽  
Caffeic Acid Phenethyl Ester ◽  
Heme Oxygenase 1 ◽  
Human Endothelial Cells

scholarly journals PGC1α Regulates the Endothelial Response to Fluid Shear Stress via Telomerase Reverse Transcriptase Control of Heme Oxygenase-1

2021 ◽  
Author(s):  
Shashi Kant ◽  
Khanh-Van Tran ◽  
Miroslava Kvandova ◽  
Amada D. Caliz ◽  
Hyung-Jin Yoo ◽  
...  
Keyword(s):  
Shear Stress ◽  
Reverse Transcriptase ◽  
Heme Oxygenase ◽  
Fluid Shear Stress ◽  
Heme Oxygenase 1 ◽  
Telomerase Reverse Transcriptase ◽  
Fluid Shear ◽  
Flow Alignment

Fluid shear stress (FSS) is known to mediate multiple phenotypic changes in the endothelium. Laminar FSS (undisturbed flow) is known to promote endothelial alignment to flow that is key to stabilizing the endothelium and rendering it resistant to atherosclerosis and thrombosis. The molecular pathways responsible for endothelial responses to FSS are only partially understood. Here we have identified peroxisome proliferator gamma coactivator-1α (PGC-1α) as a flow-responsive gene required for endothelial flow alignment in vitro and in vivo. Compared to oscillatory FSS (disturbed flow) or static conditions, laminar FSS (undisturbed flow) increased PGC-1α expression and its transcriptional co-activation. PGC-1α was required for laminar FSS-induced expression of telomerase reverse transcriptase (TERT) in vitro and in vivo via its association with ERRα and KLF4 on the TERT promoter. We found that TERT inhibition attenuated endothelial flow alignment, elongation, and nuclear polarization in response to laminar FSS in vitro and in vivo. Among the flow-responsive genes sensitive to TERT status was heme oxygenase-1 (HMOX1), a gene required for endothelial alignment to laminar FSS. Thus, these data suggest an important role for a PGC-1α-TERT-HMOX1 axis in the endothelial stabilization response to laminar FSS.

Role of p120-catenin in the morphological changes of endothelial cells exposed to fluid shear stress

2010 ◽  
Vol 398 (3) ◽  
pp. 426-432 ◽  
Author(s):  
Naoya Sakamoto ◽  
Kei Segawa ◽  
Makoto Kanzaki ◽  
Toshiro Ohashi ◽  
Masaaki Sato
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Morphological Changes ◽  
Fluid Shear ◽  
P120 Catenin

scholarly journals PGC1α Regulates the Endothelial Response to Fluid Shear Stress via Telomerase Reverse Transcriptase Control of Heme Oxygenase-1

2021 ◽  
Author(s):  
Shashi Kant ◽  
Khanh-Van Tran ◽  
Miroslava Kvandova ◽  
Amada D. Caliz ◽  
Hyung-Jin Yoo ◽  
...  
Keyword(s):  
Shear Stress ◽  
Reverse Transcriptase ◽  
Heme Oxygenase ◽  
Fluid Shear Stress ◽  
Heme Oxygenase 1 ◽  
Telomerase Reverse Transcriptase ◽  
Fluid Shear ◽  
Flow Alignment

Objective: Fluid shear stress (FSS) is known to mediate multiple phenotypic changes in the endothelium. Laminar FSS (undisturbed flow) is known to promote endothelial alignment to flow, which is key to stabilizing the endothelium and rendering it resistant to atherosclerosis and thrombosis. The molecular pathways responsible for endothelial responses to FSS are only partially understood. In this study, we determine the role of PGC1α (peroxisome proliferator gamma coactivator-1α)-TERT (telomerase reverse transcriptase)-HMOX1 (heme oxygenase-1) during shear stress in vitro and in vivo. Approach and Results: Here, we have identified PGC1α as a flow-responsive gene required for endothelial flow alignment in vitro and in vivo. Compared with oscillatory FSS (disturbed flow) or static conditions, laminar FSS (undisturbed flow) showed increased PGC1α expression and its transcriptional coactivation. PGC1α was required for laminar FSS-induced expression of TERT in vitro and in vivo via its association with ERRα(estrogen-related receptor alpha) and KLF (Kruppel-like factor)-4 on the TERT promoter. We found that TERT inhibition attenuated endothelial flow alignment, elongation, and nuclear polarization in response to laminar FSS in vitro and in vivo. Among the flow-responsive genes sensitive to TERT status, HMOX1 was required for endothelial alignment to laminar FSS. Conclusions: These data suggest an important role for a PGC1α-TERT-HMOX1 axis in the endothelial stabilization response to laminar FSS.

scholarly journals Fluid shear stress modulates endothelial inflammation by targeting LIMS2

2020 ◽  
Vol 245 (18) ◽  
pp. 1656-1663
Author(s):  
Junyao Wang ◽  
Shiyanjin Zhang
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Inflammatory Factors ◽  
Zinc Finger Domain ◽  
Human Endothelial Cells ◽  
Fluid Shear ◽  
Endothelial Inflammation

Mechanosensitive genes regulate multiple cardiovascular pathophysiological processes and disorders; however, the role of flow-sensitive genes in atherosclerosis is still unknown. In this study, we identify LIM Zinc Finger Domain Containing 2 (LIMS2) that acts as a mechanosensitive gene downregulated by disturbed flow (d-flow) both in human endothelial cells (ECs) in vitro and in mice in vivo. Mechanistically, d-flow suppresses LIMS2 expression, which leads to endothelial inflammation by upregulating typical inflammatory factors, VCAM-1, and ICAM-1 in human ECs. The findings indicate that LIMS2, the new flow-sensitive gene, may help us to find a new insight to explain how d-flow caused endothelial inflammation and provide a new therapeutic approach for atherosclerosis in the future.

Sign in / Sign up

Export Citation Format

Share Document