Regulation of Neointimal Morphogenesis by Blood Shear Stress

2000 ◽  
Author(s):  
Shu Q. Liu
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Biological Processes

Abstract Blood vessels are subject to blood shear stress, which influences vascular biological processes [1]. Here the author investigates how blood shear stress regulates neointimal morphogenesis in blood vessels.

The molecular mechanism of mechanotransduction in vascular homeostasis and disease

2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Vascular Diseases ◽  
Cell Interactions ◽  
Aortic Aneurysms ◽  
Cyclic Stretch ◽  
Mechanical Stimuli ◽  
Vascular Homeostasis ◽  
Matrix Cell

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.

Numerical Investigation and Prediction of Atherogenic Sites in Branching Arteries

1995 ◽  
Vol 117 (3) ◽  
pp. 350-357 ◽  
Author(s):  
M. Lei ◽  
C. Kleinstreuer ◽  
G. A. Truskey
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Blood Vessels ◽  
Vector Fields ◽  
Stress Gradient ◽  
Western World ◽  
Medium Size ◽  
Wall Shear Stress Gradient ◽  
Shear Stress Gradient ◽  
Wall Shear

Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the US and most of the western world. It is widely accepted that the focal nature of the disease in arterial bends, junctions, and bifurcations is directly related to locally abnormal hemodynamics, often labeled “disturbed flows.” Employing the aorto-celiac junction of rabbits as a representative atherosclerotic model and considering other branching blood vessels with their distinctive input wave forms, it is suggested that the local wall shear stress gradient (WSSG) is the single best indicator of nonuniform flow fields leading to atherogenesis. Alternative predictors of susceptible sites are briefly evaluated. The results discussed include transient velocity vector fields, wall shear stress gradient distributions, and a new dimensionless parameter for the prediction of the probable sites of stenotic developments in branching blood vessels. Some of the possible underlying biological aspects of atherogenesis due to locally significant |WSSG|-magnitudes are briefly discussed.

An Innovative Ex Vivo Vascular Bioreactor as Comprehensive Tool to Study the Behavior of Native Blood Vessels Under Physiologically Relevant Conditions

2019 ◽  
Vol 2 (4) ◽  
Author(s):  
Noemi Vanerio ◽  
Marco Stijnen ◽  
Bas A. J. M. de Mol ◽  
Linda M. Kock
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Ultrasound Imaging ◽  
Ex Vivo ◽  
Biological Response ◽  
Vessel Diameter ◽  
Tissue Growth ◽  
In Vivo Models

Abstract Ex vivo systems represent important models to study vascular biology and to test medical devices, combining the advantages of in vitro and in vivo models such as controllability of parameters and the presence of biological response, respectively. The aim of this study was to develop a comprehensive ex vivo vascular bioreactor to long-term culture and study the behavior of native blood vessels under physiologically relevant conditions. The system was designed to allow for physiological mechanical loading in terms of pulsatile hemodynamics, shear stress, and longitudinal prestretch and ultrasound imaging for vessel diameter and morphology evaluation. In this first experience, porcine carotid arteries (n = 4) from slaughterhouse animals were cultured in the platform for 10 days at physiological temperature, CO2 and humidity using medium with blood-mimicking viscosity, components, and stability of composition. As expected, a significant increase in vessel diameter was observed during culture. Flow rate was adjusted according to diameter values to reproduce and maintain physiological shear stress, while pressure was kept physiological. Ultrasound imaging showed that the morphology and structure of cultured arteries were comparable to in vivo. Histological analyses showed preserved endothelium and extracellular matrix and neointimal tissue growth over 10 days of culture. In conclusion, we have developed a comprehensive pulsatile system in which a native blood vessel can be cultured under physiological conditions. The present model represents a significant step toward ex vivo testing of vascular therapies, devices, drug interaction, and as basis for further model developments.

High Glucose Alters Endothelial Cell Response to Shear Stress

2009 ◽  
Author(s):  
Steven F. Kemeny ◽  
Alisa Morss Clyne
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Cell Mechanics ◽  
High Glucose ◽  
Fluid Shear Stress ◽  
Cell Function ◽  
Focal Adhesions ◽  
Endothelial Cell Function

Endothelial cells line the walls of all blood vessels, where they maintain homeostasis through control of vascular tone, permeability, inflammation, and the growth and regression of blood vessels. Endothelial cells are mechanosensitive to fluid shear stress, elongating and aligning in the flow direction [1–2]. This shape change is driven by rearrangement of the actin cytoskeleton and focal adhesions [2]. Hyperglycemia, a hallmark of diabetes, affects endothelial cell function. High glucose has been shown to increase protein kinase C, formation of glucose-derived advanced glycation end-products, and glucose flux through the aldose reductase pathway within endothelial cells [3]. These changes are thought to be related to increased reactive oxygen species production [4]. While endothelial cell mechanics have been widely studied in healthy conditions, many disease states have yet to be explored. Biochemical alterations related to high glucose may alter endothelial cell mechanics.

scholarly journals PO-277 Nitric oxide generation in red blood cells induced by exercise

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Zhenghui Zha ◽  
Yuli Zhang
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Red Blood Cells ◽  
Blood Vessels ◽  
Blood Cells ◽  
White Blood Cells ◽  
Pi3k Pathway ◽  
No Production ◽  
Hemodynamic Changes ◽  
Enzyme Source

Objective Vascular endothelial nitric oxide synthase (NOS) is considered to be the main enzyme source for NO production in blood vessels, and studies have shown that RBC may also express NOS and produce NO. The purpose of this study was to summarize the expression of NOS in vascular red blood cells caused by changes in hemodynamics, and to improve the bioavailability of NO, and to lay a theoretical foundation for exploring the mechanism of exercise to improve vasodilation. Methods A literature review method was used to analyze related studies on exercise and RBC-NOS published in recent years. Results Intravascular NO is one of the most important vascular signaling molecules, which has the function of relaxing blood vessels. NO is produced during the conversion of L-arginine into L-citrulline, which is mainly dependent on the regulation of vascular eNOS. RBC can express NOS under certain action, and RBC-NOS is mainly located on RBC membrane and cytoplasm; The regulatory mechanisms of RBC-NOS and eNOS have similarities and differences: RBC-NOS and eNOS are both dependent on Ca2+ regulation and phosphorylation of Serine 1177  via the PI3K pathway; however, since red blood cells do not have nuclei, endoplasmic reticulum and Golgi, they do not have other mechanisms of action of eNOS. Therefore, the vascular endothelium is not the only source of NO production. Red blood cells, white blood cells and platelets can produce NO. The amount of NO produced by red blood cells is significantly higher than that of white blood cells and platelets，it is another major source of NO production in blood vessels.The level of wall shear stress is the main determinant of NOS expression in blood vessels: On the one hand, exercise training can cause hemodynamic changes, increased shear stress, and induce changes in eNOS and RBC-NOS levels, increase NO bioavailability, and participate in the regulation of vasodilation.On the other hand, moderate-intensity exercise causes NO produced by RBC to increase red blood cell deformability and participate in vascular regulation. Conclusions 1.Erythrocyte is an enzyme source that relies on hemodynamics to release NO from the blood vessel wall. It is regulated by Ca2+ and phosphorylates ser1177 through the PI3K pathway to participate in the regulation of the body. 2.Hemodynamic changes caused by exercise training can simultaneously induce the expression of eNOS and RBC-NOS, increase the bioavailability of NO, and jointly mediate vasodilation.

Influence of Intermittent Pneumatic Compression on Wall Shear Stress and Nitric Oxide Levels

2011 ◽  
Author(s):  
Ganesh Swaminathan ◽  
Suraj Thyagaraj ◽  
Francis Loth ◽  
Susan McCormick ◽  
Hisham Bassiouny
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Blood Vessels ◽  
Healthy Subjects ◽  
Vascular Diseases ◽  
Intermittent Pneumatic Compression ◽  
Peripheral Vascular ◽  
Peripheral Vascular Diseases ◽  
Wall Shear

Wall shear stress (WSS) in blood vessels has been shown to play an important role in the development of atherosclerosis. In particular, regions of low and oscillating WSS have been shown to correlate with the localization of atherosclerosis. Thus, we hypothesize that increasing the WSS for patients with peripheral vascular diseases (PVD) will either reduce PVD severity or slow its progression. We analyzed WSS changes from a study by Delis et al. on 32 limbs of PVD patients [1]. Results show that intermittent pneumatic compression (IPC) increases mean WSS by 170% and 240% in PVD patients and healthy subjects, respectively. Peak WSS was found to increase by 93% and 40% in PVD patients and healthy subjects, respectively. In addition, we examined changes in NOX level with use of IPC on five limbs from PVD patients. Our study demonstrated increased NOx levels in subjects after IPC. Further research is needed to determine the benefits of IPC for PVD patients.

scholarly journals Assessment of the Effects of Bisphenol A on Dopamine Synthesis and Blood Vessels in the Goldfish Brain

2019 ◽  
Vol 20 (24) ◽  
pp. 6206 ◽  
Author(s):  
Qing Wang ◽  
Fangmei Lin ◽  
Qi He ◽  
Xiaochun Liu ◽  
Shiqiang Xiao ◽  
...  
Keyword(s):  
Shear Stress ◽  
Bisphenol A ◽  
Blood Vessels ◽  
Fluid Shear Stress ◽  
Dopamine Neurons ◽  
Dopamine Synthesis ◽  
Exposure Group ◽  
Fluid Shear ◽  
Toxicological Studies ◽  
The Brain

Bisphenol A (BPA) is an abundant contaminant found in aquatic environments. While a large number of toxicological studies have investigated the effects of BPA, the potential effects of BPA exposure on fish brain have rarely been studied. To understand how BPA impacts goldfish brains, we performed a transcriptome analysis of goldfish brains that had been exposed to 50 μg L−1 and 0 μg L−1 BPA for 30 days. In the analysis of unigene expression profiles, 327 unigenes were found to be upregulated and 153 unigenes were found to be downregulated in the BPA exposure group compared to the control group. Dopaminergic signaling pathway-related genes were significantly downregulated in the BPA exposure group. Furthermore, we found that serum dopamine concentrations decreased and TUNEL (terminal deoxynucleotidyl transferase 2-deoxyuridine, 5-triphosphate nick end labeling) staining was present in dopamine neurons enriched regions in the brain after BPA exposure, suggesting that BPA may disrupt dopaminergic processes. A KEGG analysis revealed that genes involved in the fluid shear stress and atherosclerosis pathway were highly significantly enriched. In addition, the qRT-PCR results for fluid shear stress and atherosclerosis pathway-related genes and the vascular histology of the brain showed that BPA exposure could damage blood vessels and induce brain atherosclerosis. The results of this work provide insights into the biological effects of BPA on dopamine synthesis and blood vessels in goldfish brain and could lay a foundation for future BPA neurotoxicity studies.

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