Laminar Shear Stress Promotes Vascular Endothelial Cell Autophagy Through Upregulation with Rab4

2016 ◽  
Vol 35 (3) ◽  
pp. 118-123 ◽  
Author(s):  
Pingbo Yao ◽  
Hong Zhao ◽  
Wenjuan Mo ◽  
Pingping He
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear

scholarly journals Rac1 mediates laminar shear stress-induced vascular endothelial cell migration

2013 ◽  
Vol 7 (6) ◽  
pp. 472-478 ◽  
Author(s):  
Xianliang Huang ◽  
Yang Shen ◽  
Yi Zhang ◽  
Lin Wei ◽  
Yi Lai ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear

Wound Closure in Sheared Endothelial Cells is Enhanced by Modulation of Vascular Endothelial-Cadherin Expression and Localization

2002 ◽  
Vol 227 (11) ◽  
pp. 1006-1016 ◽  
Author(s):  
Maria Luiza C. Albuquerque ◽  
Annette S. Flozak
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Protein Expression ◽  
Wound Closure ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Static Conditions ◽  
Laminar Shear ◽  
Cell Cell

We previously demonstrated that laminar shear stress enhances human coronary artery endothelial cell (HCAEC) wound closure via the mechanisms of cell spreading and migration. Because cell–cell junctional proteins such as vascular endothelial cell cadherin (VE–cadherin) are critical to cell–cell adhesion and motility, we tested the hypothesis that modulation of VE–cadherin expression under shear stress may be linked to this enhancement in wound closure. HCAEC monolayers were preconditioned to attain cellular alignment by shearing at 12 dynes/cm2 for 18 hr in a parallel-plate flow chamber. Subsequently, they were divided into the following three groups: (i) control; (ii) treated with anti-cadherin-5 antibody; or (iii) treated with the calcium chelating agent EGTA. Next, the monolayers were wounded with a metal spatula and resheared at 20 dynes/cm2 or left static. Time-lapse imaging was performed during the first 3 hr after imposition of these conditions, immunocytochemistry or Western blot analyses for VE–cadherin expression were performed on all wounded monolayers. Deconvolution microscopy, three-dimensional cell–cell junctional reconstruction images, and histogram analyses of interendothelial junction signal intensities were performed on cells at the wound edge of a monolayer. Under shear, HCAEC demonstrated increased VE–cadherin immunofluorescence and protein expression despite an enhancement in wound closure compared with static conditions. In separate experiments, application with anti-cadherin-5 antibody or treatment with EGTA attenuated VE–cadherin expression and further enhanced wound closure compared with control shear and all static conditions. In addition, the pattern of VE–cadherin localization with these treatments became more intracellular and nuclear in appearance. These findings of changes in this junctional adhesion protein expression and localization may further our understanding of laminar shear stress-induced endothelial repair in the coronary circulation.

scholarly journals SENCR stabilizes vascular endothelial cell adherens junctions through interaction with CKAP4

2018 ◽  
Vol 116 (2) ◽  
pp. 546-555 ◽  
Author(s):  
Qing Lyu ◽  
Suowen Xu ◽  
Yuyan Lyu ◽  
Mihyun Choi ◽  
Christine K. Christie ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Adherens Junctions ◽  
Vascular Endothelial Cell ◽  
Membrane Integrity ◽  
Laminar Shear Stress ◽  
Loss Of Function ◽  
Laminar Shear

SENCR is a human-specific, vascular cell-enriched long-noncoding RNA (lncRNA) that regulates vascular smooth muscle cell and endothelial cell (EC) phenotypes. The underlying mechanisms of action of SENCR in these and other cell types is unknown. Here, levels of SENCR RNA are shown to be elevated in several differentiated human EC lineages subjected to laminar shear stress. Increases in SENCR RNA are also observed in the laminar shear stress region of the adult aorta of humanized SENCR-expressing mice, but not in disturbed shear stress regions. SENCR loss-of-function studies disclose perturbations in EC membrane integrity resulting in increased EC permeability. Biotinylated RNA pull-down and mass spectrometry establish an abundant SENCR-binding protein, cytoskeletal-associated protein 4 (CKAP4); this ribonucleoprotein complex was further confirmed in an RNA immunoprecipitation experiment using an antibody to CKAP4. Structure–function studies demonstrate a noncanonical RNA-binding domain in CKAP4 that binds SENCR. Upon SENCR knockdown, increasing levels of CKAP4 protein are detected in the EC surface fraction. Furthermore, an interaction between CKAP4 and CDH5 is enhanced in SENCR-depleted EC. This heightened association appears to destabilize the CDH5/CTNND1 complex and augment CDH5 internalization, resulting in impaired adherens junctions. These findings support SENCR as a flow-responsive lncRNA that promotes EC adherens junction integrity through physical association with CKAP4, thereby stabilizing cell membrane-bound CDH5.

15-Deoxy-Δ12,14-prostaglandin J2 and laminar fluid shear stress stabilize c-IAP1 in vascular endothelial cells

2003 ◽  
Vol 285 (1) ◽  
pp. H38-H46 ◽  
Author(s):  
Yoji Taba ◽  
Megumi Miyagi ◽  
Yoshikazu Miwa ◽  
Hiroyasu Inoue ◽  
Fumi Takahashi-Yanaga ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Expression Level ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Endothelial Cell Apoptosis ◽  
Laminar Shear

Laminar shear stress strongly inhibits vascular endothelial cell apoptosis by unknown mechanisms. We reported that shear stress stimulates endothelial cells to produce 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) by elevating the expression level of lipocalin-type prostaglandin D synthase. To investigate the role of 15d-PGJ2 produced in the vascular wall, we examined the effect of 15d-PGJ2 on endothelial cell apoptosis. We induced apoptosis in human umbilical vein endothelial cells (HUVECs) by growth factor deprivation. 15d-PGJ2 strongly inhibited DNA ladder formation, nuclear fragmentation, and caspase-3-like activity in HUVECs. To elucidate the mechanism by which 15d-PGJ2 inhibits endothelial cell apoptosis, we examined expression of the inhibitor of apoptosis proteins (IAP) cellular-IAP1 (c-IAP1), c-IAP2, x-linked IAP, and survivin in HUVECs. In parallel with the inhibition of apoptosis, 15d-PGJ2 elevated the expression level of c-IAP1 protein in a dose- and time-dependent manner without changing the mRNA level. Laminar shear stress also induced c-IAP1 expression. Chase experiments with the use of cycloheximide revealed that 15d-PGJ2 and shear stress both inhibited the proteolytic degradation of c-IAP1 protein. These results suggested that 15d-PGJ2 inhibits endothelial cell apoptosis through, at least in part, c-IAP1 protein stabilization. This mechanism might be involved in the antiapoptotic effect of laminar shear stress.

scholarly journals Turbulent fluid shear stress induces vascular endothelial cell turnover in vitro.

1986 ◽  
Vol 83 (7) ◽  
pp. 2114-2117 ◽  
Author(s):  
P. F. Davies ◽  
A. Remuzzi ◽  
E. J. Gordon ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Turnover ◽  
Fluid Shear ◽  
Turbulent Fluid

scholarly journals Laminar Shear Stress Inhibits Endothelial Cell Metabolism via KLF2-Mediated Repression of PFKFB3

2015 ◽  
Vol 35 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Anuradha Doddaballapur ◽  
Katharina M. Michalik ◽  
Yosif Manavski ◽  
Tina Lucas ◽  
Riekelt H. Houtkooper ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Metabolism ◽  
Laminar Shear Stress ◽  
Laminar Shear ◽  
Endothelial Cell Metabolism

Endothelial albumin permeability is shear dependent, time dependent, and reversible

1991 ◽  
Vol 260 (6) ◽  
pp. H1992-H1996 ◽  
Author(s):  
H. Jo ◽  
R. O. Dull ◽  
T. M. Hollis ◽  
J. M. Tarbell
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluorescein Isothiocyanate ◽  
Vascular Wall ◽  
Laminar Shear Stress ◽  
Aortic Endothelial Cells ◽  
Transendothelial Permeability ◽  
Steady Laminar Shear Stress ◽  
Laminar Shear

Altered permeability of vascular endothelium to macromolecules may play a role in vascular disease as well as vascular homeostasis. Because the shear stress of flowing blood on the vascular wall is known to influence many endothelial cell properties, an in vitro system to measure transendothelial permeability (Pe) to fluorescein isothiocyanate conjugated bovine serum albumin under defined physiological levels of steady laminar shear stress was developed. Bovine aortic endothelial cells grown on polycarbonate filters pretreated with gelatin and fibronectin constituted the model system. Onset of 1 dyn/cm2 shear stress resulted in a Pe rise from 5.1 +/- 1.3 x 10(-6) cm/s to 21.9 +/- 4.6 X 10(-6) cm/s at 60 min (n = 6); while 10 dyn/cm2 shear stress increased Pe from 4.8 +/- 1.5 X 10(-6) cm/s to 50.2 +/- 6.8 X 10(-6) cm/s at 30 min and 49.6 +/- 8.9 X 10(-6) cm/s at 60 (n = 9). Pe returned to preshear values within 120 and 60 min after removal of 1 and 10 dyn/cm2 shear stress, respectively. The data show that endothelial cell Pe in vitro is acutely sensitive to shear stress.

Sign in / Sign up

Export Citation Format

Share Document