Differential effects of orbital and laminar shear stress on endothelial cells

Dardik, Alan; Chen, Leiling; Frattini, Jared C.; Asada, Hidenori; Aziz, Faisal; Kudo, Fabio A.; Sumpio, Bauer E.

doi:10.1016/j.jvs.2005.01.020

Cited by 283 publications

(286 citation statements)

References 49 publications

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“…In addition, cultures exposed to physiologically low rates of flow yield gene expression profiles similar to endothelium from atherosclerotic-prone arteries (e.g. carotid bifurcations) (Dardik, 2005;Brooks et al, 2004;Resnick, 1997;Wasserman and Topper, 2004) and also show higher levels of endothelial apoptosis (Tricot, 2000). In the present study a model is proposed for a unique vascular structure, in which there is a circulatory input (visualised by 150 kDa FITC-dextran) but very low flow and therefore the shear stress is also low.…”

Section: Discussionmentioning

confidence: 85%

“…Within vessels containing both an inlet and outlet, shear forces on the endothelial cells are key regulators of vascular segment survival (Meeson, 1996;Azmi and O'Shea, 1984). Low flow rates in EC cultures have been shown to result in alterations in the distribution of cytoskeletal proteins (Dardik, 2005) and morphology (Malek, 1993) and induction of tissue factor expression, the cell surface initiator protein for the haemostatic cascade. In addition, cultures exposed to physiologically low rates of flow yield gene expression profiles similar to endothelium from atherosclerotic-prone arteries (e.g.…”

Section: Discussionmentioning

confidence: 99%

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Experimental and theoretical modelling of blind-ended vessels within a developing angiogenic plexus

Guerreiro-Lucas

Pop

Machado

et al. 2008

Microvascular Research

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Angiogenic sprouts at the leading edge of an expanding vascular plexus are recognised as major regulators of the structure of the developing network. Early in sprout development, a vascular lumen is often evident which communicates with the parent vessel while the distal tip is blind-ended. Here we describe the temporal evolution of blind-ended vessels (BEVs) in a small wound made in the panniculus carnosus muscle of a mouse viewed in a dorsal skin-fold window-chamber model with intra-vital microscopy during the most active period of angiogenesis (days 5-8 after injury). Although these structures have been mentioned anecdotally in previous studies, we observed BEVs to be frequent, albeit transient, features of plexus formation. Plasma leakage into the surrounding extracellular matrix occurring from these immature conduits could play an important role in preparing hypoxic tissue for vascular invasion. Although sprout growth is likely to be regulated by its flow environment, the parameters regulating flow into and through BEVs have not been characterised in situ. Longitudinal data from individual animals show that the number of BEVs filled with plasma alone peaks at day 7, when they can exceed 150 μm in length. Additionally, BEVs greater than 40 μm in length are more likely to be filled with stationary erythrocytes than with plasma alone. Using a mathematical model, we show how the flux of 150kD fluorinated (FITC-) dextran through an individual plasma-filled BEV is related to its geometry being determined primarily by its surface area; by fitting theoretical intensity values to experimental data we assess the permeability of the vessel to FITC-dextran. Plasma skimming provides a mechanistic explanation for the observation that BEVs with larger surface area are more likely to recruit erythrocytes.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Experimental and theoretical modelling of blind-ended vessels within a developing angiogenic plexus

Guerreiro-Lucas

Pop

Machado

et al. 2008

Microvascular Research

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“…Fluid flow was applied to confluent cultures with an orbital shaker (Lab-Line, Melrose Park, IL) (32)(33)(34). Although this technique does not result in uniform application of laminar shear stress across the entire monolayer, the majority of the cells are exposed to near maximal shear stress ( max ), which can be calculated as…”

Section: Application Of Fluid Shear Stressmentioning

confidence: 99%

MAPKs (ERK½, p38) and AKT Can Be Phosphorylated by Shear Stress Independently of Platelet Endothelial Cell Adhesion Molecule-1 (CD31) in Vascular Endothelial Cells

Sumpio

Yun

Córdova

et al. 2005

Journal of Biological Chemistry

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“…It is believed that risk factors induce EC apoptosis, leading to the denudation or dysfunction of the intact endothelial monolayer, which causes lipid accumulation, monocyte adhesion, and inflammatory reactions that initiate atherosclerotic lesion (5,(9)(10)(11)(12). Although information on risk factorinduced atherosclerosis has been accumulating, the underlying mechanism remains unclear.…”

mentioning

confidence: 99%

Sustained activation of XBP1 splicing leads to endothelial apoptosis and atherosclerosis development in response to disturbed flow

Zeng

Zampetaki

Margariti

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

196

184

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X-box binding protein 1 (XBP1) is a key signal transducer in endoplasmic reticulum stress response, and its potential role in the atherosclerosis development is unknown. This study aims to explore the impact of XBP1 on maintaining endothelial integrity related to atherosclerosis and to delineate the underlying mechanism. We found that XBP1 was highly expressed at branch points and areas of atherosclerotic lesions in the arteries of ApoE ؊/؊ mice, which was related to the severity of lesion development. In vitro study using human umbilical vein endothelial cells (HUVECs) indicated that disturbed flow increased the activation of XBP1 expression and splicing. Overexpression of spliced XBP1 induced apoptosis of HUVECs and endothelial loss from blood vessels during ex vivo cultures because of caspase activation and down-regulation of VE-cadherin resulting from transcriptional suppression and matrix metalloproteinase-mediated degradation. Reconstitution of VEcadherin by Ad-VEcad significantly increased Ad-XBP1s-infected HUVEC survival. Importantly, Ad-XBP1s gene transfer to the vessel wall of ApoE ؊/؊ mice resulted in development of atherosclerotic lesions after aorta isografting. These results indicate that XBP1 plays an important role in maintaining endothelial integrity and atherosclerosis development, which provides a potential therapeutic target to intervene in atherosclerosis.caspase ͉ endothelial integrity ͉ Ve-cadherin ͉ vessel graft ͉ mouse model A therosclerosis is a leading cause of death worldwide (1, 2).Accumulating evidence suggests that atherosclerosis is a multifactorial disease that can be initiated by risk factors (3-6). An important feature of atherosclerosis is its geographic distribution along the artery wall, i.e., occurring more frequently at curved or branching points in the vasculature, indicating that the flow pattern exerts an important role in the development of atherosclerotic lesions (7,8).Endothelial cells (ECs) are key cellular components of blood vessels, functioning as selectively permeable barriers between blood and tissues. It is believed that risk factors induce EC apoptosis, leading to the denudation or dysfunction of the intact endothelial monolayer, which causes lipid accumulation, monocyte adhesion, and inflammatory reactions that initiate atherosclerotic lesion (5, 9-12). Although information on risk factorinduced atherosclerosis has been accumulating, the underlying mechanism remains unclear.The X-box binding protein 1 (XBP1) was originally identified as a bZIP protein capable of binding to the cis-acting X box present in the promoter regions of human major histocompatibility complex class II genes (13) and is known to be essential for liver growth and B lymphocyte differentiation (14,15). In mammalian cells, XBP1 is a key signal transducer in the endoplasmic reticulum (ER) stress response. It has also been reported that there is a link between XBP1 and human disease (16,17). Although ER stress is reported to be involved in atherosclerosis (18)(19)(20)(21)(22), the role of XB...

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Differential effects of orbital and laminar shear stress on endothelial cells

Cited by 283 publications

References 49 publications

Experimental and theoretical modelling of blind-ended vessels within a developing angiogenic plexus

Experimental and theoretical modelling of blind-ended vessels within a developing angiogenic plexus

MAPKs (ERK½, p38) and AKT Can Be Phosphorylated by Shear Stress Independently of Platelet Endothelial Cell Adhesion Molecule-1 (CD31) in Vascular Endothelial Cells

Sustained activation of XBP1 splicing leads to endothelial apoptosis and atherosclerosis development in response to disturbed flow

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