scholarly journals The Antiangiogenic Activity of rPAI-123Inhibits Vasa Vasorum and Growth of Atherosclerotic Plaque

2009 ◽  
Vol 104 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Mary Drinane ◽  
Jessica Mollmark ◽  
Lyubomir Zagorchev ◽  
Karen Moodie ◽  
Baiming Sun ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Vasa Vasorum ◽  
Antiangiogenic Activity

scholarly journals Antiangiogenic Activity of rPAI-123Promotes Vasa Vasorum Regression in Hypercholesterolemic Mice Through a Plasmin-Dependent Mechanism

2011 ◽  
Vol 108 (12) ◽  
pp. 1419-1428 ◽  
Author(s):  
Jessica Mollmark ◽  
Saranya Ravi ◽  
Baiming Sun ◽  
Samantha Shipman ◽  
Maarten Buitendijk ◽  
...  
Keyword(s):  
Vasa Vasorum ◽  
Antiangiogenic Activity ◽  
Dependent Mechanism

Pericyte-specific deletion of Ninjurin-1 induces fragile vasa vasorum formation and enhances intimal hyperplasia of injured vasculature

2021 ◽  
Author(s):  
Kiwamu Horiuchi ◽  
Kohei Kano ◽  
Akiho Minoshima ◽  
Taiki Hayasaka ◽  
Atsushi Yamauchi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Cytokines ◽  
Vascular Injury ◽  
Atherosclerotic Plaque ◽  
Intimal Hyperplasia ◽  
Vascular Remodeling ◽  
Three Dimensional ◽  
Vasa Vasorum ◽  
Model Mouse ◽  
Specific Deletion

Adventitial abnormalities including enhanced vasa vasorum malformation are associated with development and vulnerability of atherosclerotic plaque. However, the mechanisms of vasa vasorum malformation and its role in vascular remodeling have not been fully clarified. We recently reported that Ninjurin-1 (Ninj1) is a crucial adhesion molecule for pericytes to form matured neovessels. The purpose is to examine if Ninj1 regulate adventitial angiogenesis and affects the vascular remodeling of injured vessels using pericyte-specific Ninj1 deletion mouse model. Mouse femoral arteries were injured by insertion of coiled wire. Four weeks after vascular injury, fixed arteries were decolorized. Vascular remodeling, including intimal hyperplasia and adventitial microvessel formation were estimated in three-dimensional view. Vascular fragility, including blood leakiness was estimated by extravasation of FITC-lectin or -dextran from microvessels. Ninj1 expression was increased in pericytes in response to vascular injury. NG2-CreER/Ninj1loxp mice were treated with tamoxifen (Tam) to induce deletion of Ninj1 in pericyte (Ninj1KO). Tam-treated-NG2-CreER or Tam-nontreated NG2-CreER/Ninj1loxp mice were used as controls. Intimal hyperplasia was significantly enhanced in Ninj1KO compared with controls. Vascular leakiness was significantly enhanced in Ninj1KO. In Ninj1KO, the number of infiltrated macrophages in adventitia was increased, along with the expression of inflammatory cytokines. In conclusion, deletion of Ninj1 in pericytes induces the immature vasa vasorum formation of injured vasculature and exacerbates adventitial inflammation and intimal hyperplasia. Thus, Ninj1 contributes to the vasa vasorum maturation in response to vascular injury, and to reduction of vascular remodeling.

Abstract 1143: Imaging of Vasa Vasorum in Atherosclerotic Plaque with 99m Tc-labeled single chain-VEGF

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Satoru Ohshima ◽  
Shinichiro Fujimoto ◽  
Sotirios Tsimikas ◽  
Frank D Kolodgie ◽  
Renu Virmani ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Ex Vivo ◽  
Imaging Modality ◽  
Atherosclerotic Lesion ◽  
Vasa Vasorum ◽  
Intraplaque Hemorrhage ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Single Chain

Introduction: Adventitial vasa vasorum proliferation and neointimal neovascularization are associated with intraplaque hemorrhage, expansion of necrotic core and hence plaque vulnerability. Increased expression of VEGF and its receptors accompany neoangiogenic process. We used 99m Tc -labeled single chain VEGF (TcV) for developing potentially noninvasive imaging modality in experimentally induced aortic atherosclerotic lesion. Methods : Noninva-sive radionuclide imaging was performed with TcV (6.85 ±0. 27 mCi) in 6 NZW rabbits receiving high cholesterol diet (0.2% cholesterol, 4% fat) for one year and compared with 3 control rabbits receiving normal rabbit chow. Four hours after intravenous administration of TcV, micro SPECT/microCT imaging was performed for in vivo localization of tracer activity. Aortas were then explanted, and gamma counted for determination of % injected dose per gram (%ID/g). The aortas were then submitted for histopathologic characterization. Results : The uptake in thoracic aorta was clearly visualized non-invasively by TcV in vivo imaging in 4 of 5 rabbits in hypercholesterolemic rabbits, but not in the control animals. The %ID/g of each parts of aorta in hypercholesterolemic rabbits (Arch : 0.036 ± 0.020 %, Thoracic : 0.026 ± 0.012 %, Abd : 0.019 ± 0.009 %) was about 2.5-fold higher than that in control group (Arch : 0.014 ± 0.004 %, Thoracic : 0.009 ± 0.003 %, Abd : 0.009 ± 0.003 %) (figure a ). Ex vivo images of each group are shown as figure b . Conclusions : This preliminary study suggests a potentially novel strategy for non-invasive imaging of neoangiogenesis in atherosclerotic plaque and may allow identification of unstable plaques.

scholarly journals Atherosclerosis and Atheroma Plaque Rupture: Imaging Modalities in the Visualization of Vasa Vasorum and Atherosclerotic Plaques

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Zhonghua Sun
Keyword(s):  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Vasa Vasorum ◽  
Imaging Modalities ◽  
Cardiac Events ◽  
Adverse Cardiac Events ◽  
Atheroma Plaque ◽  
Rupture Imaging ◽  
Comprehensive Characterization

Invasive angiography has been widely accepted as the gold standard to diagnose cardiovascular pathologies. Despite its superior resolution of demonstrating atherosclerotic plaque in terms of degree of lumen stenosis, the morphological assessment for the plaque is insufficient for the analysis of plaque components, and therefore, unable to predict the risk status or vulnerability of atherosclerotic plaque. There is an increased body of evidence to show that the vasa vasorum play an important role in the initiation, progression, and complications of atherosclerotic plaque leading to major adverse cardiac events. This paper provides an overview of the evidence-based reviews of various imaging modalities with regard to their potential value for comprehensive characterization of the composition, burden, and neovascularization of atherosclerotic plaque.

scholarly journals Vasa Vasorum Restructuring in Human Atherosclerotic Plaque Vulnerability

2015 ◽  
Vol 65 (23) ◽  
pp. 2469-2477 ◽  
Author(s):  
Akira Taruya ◽  
Atsushi Tanaka ◽  
Tsuyoshi Nishiguchi ◽  
Yoshiki Matsuo ◽  
Yuichi Ozaki ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Vasa Vasorum ◽  
Plaque Vulnerability ◽  
Human Atherosclerotic Plaque

scholarly journals Mathematical Modeling of Intraplaque Neovascularization and Hemorrhage in a Carotid Atherosclerotic Plaque

2021 ◽  
Author(s):  
Y Cai ◽  
Jichao Pan ◽  
Zhiyong Li
Keyword(s):  
Atherosclerotic Plaque ◽  
Plasma Flow ◽  
Carotid Plaque ◽  
Reaction Diffusion Equations ◽  
Vasa Vasorum ◽  
Intraplaque Hemorrhage ◽  
Model Parameters ◽  
Interstitial Tissue ◽  
Plaque Progression ◽  
Imaging Data

Abstract Background Growing experimental evidence has identified neovascularization from the adventitial vasa vasorum and induced intraplaque hemorrhage (IPH) as critical indicators during the development of vulnerable atherosclerotic plaques. In this study, we propose a mathematical model incorporating intraplaque angiogenesis and hemodynamic calculation of the microcirculation, in order to obtain the quantitative evaluation of the influences of intraplaque neovascularization and hemorrhage on the vulnerable plaque development. A two-dimensional nine-point model of angiogenic microvasculature is generated based on histology of a patient’s carotid plaque. The intraplaque angiogenesis model includes three key cells (endothelial cells, smooth muscle cells and macrophages) and three key chemical factors (vascular endothelial growth factors, extracellular matrix and matrix metalloproteinase), which densities and concentrations are described by a series of reaction-diffusion equations. The hemodynamic calculation by coupling the intravascular blood flow, the extravascular plasma flow and the transvascular transport is carried out on the generated angiogenic microvessel network. We then define the IPH area by using the plasma concentration in the interstitial tissue, as well as the extravascular transport across the capillary wall. Results The simulational results reproduce a series of pathophysiological phenomena during the atherosclerotic plaque progression, such as the high microvessel density region at the shoulder areas, the enlarged necrotic core, and the IPH caused by the extravascular plasma flow across the leaky wall of the neovasculature. The simulational results show significant consistency with both the MR imaging data and in vitro experimental observations in quantity ground. Moreover, the sensitivity analysis of model parameters reveals that the IPH area and extent can be reduced significantly by decreasing the MVD and the wall permeability of the neovasculature. Conclusions The current quantitative model could help us to better understand the roles of microvascular and intraplaque hemorrhage during the carotid plaque progression.

Assessment of the vulnerable carotid atherosclerotic plaque using contrast-enhanced ultrasonography

Vascular ◽  
2016 ◽  
Vol 25 (3) ◽  
pp. 316-325 ◽  
Author(s):  
Konstantinos Filis ◽  
Levon Toufektzian ◽  
George Galyfos ◽  
Fragiska Sigala ◽  
Panagiota Kourkoveli ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Vasa Vasorum ◽  
Ultrasound Waves ◽  
Software Packages ◽  
Contrast Enhanced ◽  
Management Guidance ◽  
Contrast Enhanced Ultrasonography ◽  
Contemporary Management ◽  
Ischemic Events

Carotid atherosclerosis represents a primary cause for cerebrovascular ischemic events and its contemporary management includes surgical revascularization for moderate to severe symptomatic stenoses. However, the role of invasive therapy seems to be questioned lately for asymptomatic cases. Numerous reports have suggested that the presence of neovessels within the atherosclerotic plaque remains a significant vulnerability factor and over the last decade imaging modalities have been used to identify intraplaque neovascularization in an attempt to risk-stratify patients and offer management guidance. Contrast-enhanced ultrasonography of the carotid artery is a relatively novel diagnostic tool that exploits resonated ultrasound waves from circulating microbubbles. This property permits vascular visualization by producing superior angiography-like images, and allows the identification of vasa vasorum and intraplaque microvessels. Moreover, plaque neovascularization has been associated with plaque vulnerability and ischemic symptoms lately as well. At the same time, attempts have been made to quantify contrast-enhanced ultrasonography signal using sophisticated software packages and algorithms, and to correlate it with intraplaque microvascular density. The aim of this review was to collect all recent data on the characteristics, performance, and prognostic role of contrast-enhanced ultrasonography regarding carotid stenosis management, and to produce useful conclusions for clinical practice.

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