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intraplaque angiogenesis

Liang Guo, Raquel Fernandez, Atsushi Sakamoto, Anne Cornelissen, Ka Hyun Paek, Parker J Lee, Leah M Weinstein, Carlos J Collado-Rivera, Emanuel Harari, Robert Kutys, Torie S Samuda, Nicole A Singer, Matthew D Kutyna, Frank D Kolodgie, Renu Virmani, Aloke V Finn
Coronary artery disease remains an important cause of morbidity and mortality. Previous work, including ours, has focused on the role of intraplaque hemorrhage, particularly from immature microvessel angiogenesis, as an important contributor to plaque progression via increases in vascular permeability leading to further intraplaque hemorrhage, which increases red cell membrane-derived free cholesterol in plaque content and inflammatory cell recruitment. Evans Blue Dye (EBD) assay is widely used as a standard assay for vasculature permeability...
October 20, 2018: Bio-protocol
Shuhong Hu, Yifei Liu, Tao You, Li Zhu
Excessive neovascularization of atherosclerotic lesions increases plaque vulnerability and the susceptibility to rupture. Semaphorin 7A (Sema7A), a semaphorin family member, was recently reported to promote atherosclerotic plaque formation by mediating d-flow-induced endothelial phenotypic change and leukocyte adhesion. To extend our understanding of the proatherogenic role of Sema7A, we investigated the role of endothelial Sema7A in angiogenesis and atherosclerotic neovascularization. Sema7A overexpression in human umbilical vein endothelial cells (HUVECs) significantly upregulated VEGFA/VEGFR2 and promoted cell migration and angiogenesis...
2018: Frontiers in Physiology
Muyi Guo, Yan Cai, Chunliu He, Zhiyong Li
We propose a multiphysical mathematical model by fully coupling lipid deposition, monocytes/macrophages recruitment and angiogenesis to investigate the pathophysiological responses of an atherosclerotic plaque to the dynamic changes in the microenvironment. The time evolutions of cellular (endothelial cells, macrophages, smooth muscle cells, etc.) and acellular components (low density lipoprotein, proinflammatory cytokines, extravascular plasma concentration, etc.) within the plaque microenvironment are assessed quantitatively...
November 28, 2018: Annals of Biomedical Engineering
Daina Kashiwazaki, Keitaro Shiraishi, Shusuke Yamamoto, Tetsuhiro Kamo, Haruto Uchino, Hisayasu Saito, Naoki Akioka, Naoya Kuwayama, Kyo Noguchi, Satoshi Kuroda
BACKGROUND: Carotid endarterectomy (CEA) is known to reduce stroke risk in patients with symptomatic, moderate to severe carotid stenosis but has no apparent impact in patients with symptomatic, mild (less than 50%) carotid stenosis. However, recent development of noninvasive imaging modalities has shown that a certain subgroup of patients are at high risk for further ischemic events despite antiplatelet therapy. This study, therefore, aimed to clarify the patients' clinical features and explore the impact of CEA for them...
September 20, 2018: World Neurosurgery
Runtai Chen, Zhenchun Huang, Junyi Wang, Xiaoying Chen, Yucai Fu, Wei Wang
BACKGROUND: This study aimed to investigate the interactions between silent information regulator 1 (SIRT1) and mammalian target of rapamycin (mTOR) in intraplaque angiogenesis and their potential mechanisms through in vivo and in vitro studies. METHODS: An atherosclerosis model was established in 12 rabbits on a high-cholesterol diet. The rabbits were equally divided into 3 groups: a control group (high-lipid diet), RAP group (high-lipid diet supplemented with rapamycin) and RAP + NAM group (high-lipid diet supplemented with rapamycin and nicotinamide)...
August 2018: American Journal of the Medical Sciences
Hong Yuan, Haiqiang Hu, Jindong Sun, Mingjuan Shi, Huamin Yu, Cairong Li, Y U Sun, Zhijian Yang, Robert M Hoffman
BACKGROUND/AIM: Intraplaque neovascularization is often associated with plaque formation, development and instability, and clinical symptoms in atherosclerosis. The aim of the present study was to investigate a new strategy for treating athrosclerosis by ultrasound-targeted microbubble delivery (UTMD) targeting intraplaque neovascularization in an APOE-deficient mouse model of atherosclerosis. MATERIALS AND METHODS: A mouse model of atherosclerosis was induced by feeding Apoe-/- mice a hypercholesterolemic diet and was verified with hematoxylin and eosin staining and intercellular adhesion molecule 1 (ICAM-1) expression...
September 2018: In Vivo
Yang Mao, Xiaoqiong Liu, Yu Song, Chungang Zhai, Lei Zhang
Various angiogenic factors have been shown to play important roles in intraplaque angiogenesis, while little is known about the dynamic expression change and interplay between various angiogenic factors and intraplaque angiogenesis under high cholesterol conditions. New Zealand rabbits underwent balloon injury of the abdominal artery and then were assigned to a control group (n = 15, normal chow) or high cholesterol group (n = 25, 1% high cholesterol diet). At weeks 4, 6, 8, 10, and 12 after acclimation, rabbits (high cholesterol group, n = 5; control group, n = 3) were euthanized...
2018: PloS One
M R de Vries, L Parma, H A B Peters, A Schepers, J F Hamming, J W Jukema, M J T H Goumans, L Guo, A V Finn, R Virmani, C K Ozaki, P H A Quax
BACKGROUND: Plaque angiogenesis is associated with atherosclerotic lesion growth, plaque instability and negative clinical outcome. Plaque angiogenesis is a natural occurring process to fulfil the increasing demand of oxygen and nourishment of the vessel wall. However, inadequate formed, immature plaque neovessels are leaky and cause intraplaque haemorrhage. OBJECTIVE: Blockade of VEGFR2 normalizes the unbridled process of plaque neovessel formation and induces maturation of nascent vessels resulting in prevention of intraplaque haemorrhage and influx of inflammatory cells into the plaque and subsequently increases plaque stability...
August 13, 2018: Journal of Internal Medicine
Konstantinos Spanos, Ioannis Tzorbatzoglou, Paraskevi Lazari, Dimitrios Maras, Athanasios D Giannoukas
OBJECTIVE: The aim of the study was to determine the association of ultrasonic texture features (severity of stenosis, grey scale median, plaque area, juxtaluminal black area [JBA], and discrete white areas) previously shown to be independent predictors for stroke with established histologic features of plaque instability. METHODS: A cross-sectional study was performed involving 70 patients scheduled for carotid endarterectomy. Before surgery, carotid plaque texture features were obtained with ultrasound after normalization using commercially available software (LifeQ Medical, Nicosia, Cyprus)...
December 2018: Journal of Vascular Surgery
Daniel G Sedding, Erin C Boyle, Jasper A F Demandt, Judith C Sluimer, Jochen Dutzmann, Axel Haverich, Johann Bauersachs
Plaque microvascularization and increased endothelial permeability are key players in the development of atherosclerosis, from the initial stages of plaque formation to the occurrence of acute cardiovascular events. First, endothelial dysfunction and increased permeability facilitate the entry of diverse inflammation-triggering molecules and particles such as low-density lipoproteins into the artery wall from the arterial lumen and vasa vasorum (VV). Recognition of entering particles by resident phagocytes in the vessel wall triggers a maladaptive inflammatory response that initiates the process of local plaque formation...
2018: Frontiers in Immunology
Muyi Guo, Yan Cai, Xinke Yao, Zhiyong Li
Observational studies have identified angiogenesis from the adventitial vasa vasorum and intraplaque hemorrhage (IPH) as critical factors in atherosclerotic plaque progression and destabilization. Here we propose a mathematical model incorporating intraplaque neovascularization and hemodynamic calculation with plaque destabilization for the quantitative evaluation of the role of neoangiogenesis and IPH in the vulnerable atherosclerotic plaque formation. An angiogenic microvasculature is generated by two-dimensional nine-point discretization of endothelial cell proliferation and migration from the vasa vasorum...
August 7, 2018: Journal of Theoretical Biology
Ru Ying, Sheng-Wei Li, Jia-Yuan Chen, Hai-Feng Zhang, Ying Yang, Zhen-Jie Gu, Yang-Xin Chen, Jing-Feng Wang
BACKGROUND: Perivascular adipose tissue (PVAT) accelerates plaque progression and increases cardiovascular risk. We tested the hypothesis that PVAT contributed to plaque vulnerability and investigated whether endoplasmic reticulum stress (ER stress) in PVAT played an important role in vulnerable plaque. METHODS: We transplanted thoracic aortic PVAT or subcutaneous adipose tissue as a control, from donor mice to carotid arteries of recipient apolipoprotein E deficient (apoE-/- ) mice after removing carotid artery collar placed for 6 weeks...
April 18, 2018: Journal of Translational Medicine
Yan Sun, Xiao-Li Liu, Dai Zhang, Fang Liu, Yu-Jing Cheng, Yue Ma, Yu-Jie Zhou, Ying-Xin Zhao
BACKGROUND: Intraplaque angiogenesis, the process of generating new blood vessels mediated by endothelial cells, contributes to plaque growth, intraplaque hemorrhage, and thromboembolic events. Platelet-derived exosomes (PLT-EXOs) affect angiogenesis in multiple ways. The ability of miR-126, one of the best-characterized miRNAs that regulates angiogenesis, carried by PLT-EXOs to influence angiogenesis via the regulation of the proliferation and migration of endothelial cells is unknown...
March 13, 2018: Current Vascular Pharmacology
Etsu Suzuki, Hiroyuki Imuta, Daishi Fujita, Masao Takahashi, Shigeyoshi Oba, Arihiro Kiyosue, Hiroaki Nishimatsu
BACKGROUND: Intraplaque hemorrhage (IPH) has been implicated in plaque instability and rupture in atherosclerotic lesions, although the mechanisms by which IPH progresses remain largely unknown. In this study, apolipoprotein E-deficient mice with carotid artery ligation and cuff placement around the artery were used, and pro-inflammatory cytokines that are implicated in IPH were analyzed.Methods and Results:The expression of interleukin-1β (IL-1β) increased significantly following cuff placement compared with mice with carotid artery ligation alone...
March 23, 2018: Circulation Journal: Official Journal of the Japanese Circulation Society
Liang Guo, Hirokuni Akahori, Emanuel Harari, Samantha L Smith, Rohini Polavarapu, Vinit Karmali, Fumiyuki Otsuka, Rachel L Gannon, Ryan E Braumann, Megan H Dickinson, Anuj Gupta, Audrey L Jenkins, Michael J Lipinski, Johoon Kim, Peter Chhour, Paul S de Vries, Hiroyuki Jinnouchi, Robert Kutys, Hiroyoshi Mori, Matthew D Kutyna, Sho Torii, Atsushi Sakamoto, Cheol Ung Choi, Qi Cheng, Megan L Grove, Mariem A Sawan, Yin Zhang, Yihai Cao, Frank D Kolodgie, David P Cormode, Dan E Arking, Eric Boerwinkle, Alanna C Morrison, Jeanette Erdmann, Nona Sotoodehnia, Renu Virmani, Aloke V Finn
Intake of hemoglobin by the hemoglobin-haptoglobin receptor CD163 leads to a distinct alternative non-foam cell antiinflammatory macrophage phenotype that was previously considered atheroprotective. Here, we reveal an unexpected but important pathogenic role for these macrophages in atherosclerosis. Using human atherosclerotic samples, cultured cells, and a mouse model of advanced atherosclerosis, we investigated the role of intraplaque hemorrhage on macrophage function with respect to angiogenesis, vascular permeability, inflammation, and plaque progression...
March 1, 2018: Journal of Clinical Investigation
Benoit Pourcet, Bart Staels
Atherosclerosis is a chronic inflammatory disease of the vasculature that is initiated by cholesterol deposition into the arterial wall, which triggers the infiltration of immune and inflammatory cells, including monocytes and macrophages. As atherosclerotic plaques progress, localized hypoxia promotes compensatory angiogenesis from the vasa vasorum. Immature neovessels are prone to leakage, thus destabilizing the plaque and leading to intraplaque hemorrhage. Macrophages with different phenotypes, ranging from classical inflammatory subtypes to alternatively activated antiinflammatory macrophages, have been identified in atherosclerotic lesions...
March 1, 2018: Journal of Clinical Investigation
Bieke Van Der Veken, Guido De Meyer, Wim Martinet
No abstract text is available yet for this article.
August 2017: Atherosclerosis
Bieke Van Der Veken, Guido De Meyer, Wim Martinet
No abstract text is available yet for this article.
August 2017: Atherosclerosis
Wen Wu, Xiaobo Li, Guangfeng Zuo, Jiangqin Pu, Xinlei Wu, Shaoliang Chen
Angiogenesis is described as a sprouting and growth process of new blood vessels from pre-existing vasculature. The relationship between angiogenesis and coronary artery disease (CAD) is double-sided. On one hand, angiogenesis within plaques is responsible for facilitating the growth and vulnerability of plaques by causing intraplaque hemorrhage and inflammatory cell influx, and overabundance of erythrocytes and inflammatory cells within a plaque probably causes plaque rupture, further leading to acute coronary syndrome...
2018: Current Pharmaceutical Design
Sara Shoeibi, Paul Mozdziak, Shabnam Mohammadi
Angiogenesis is a complex process of budding, the formation of new blood vessels from pre-existing microvessels, via migration, proliferation and survival. Vascular angiogenesis factors include different classes of molecules that have a fundamental role in blood vessel formation. Numerous inducers of angiogenesis, such as the members of the vascular endothelial growth factor (VEGF) family, basic fibroblast growth factor (bFGF), angiopoietin (Ang), hepatocyte growth factor (HGF), and hypoxia inducible factor-1 (HIF-1), have an important role in angiogenesis...
May 2018: Microvascular Research
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