scholarly journals A neutralizing IL-11 antibody reduces vessel hyperplasia in a mouse carotid artery wire injury model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
David Schumacher ◽  
Elisa A. Liehn ◽  
Pakhwan Nilcham ◽  
David Castaño Mayan ◽  
Chutima Rattanasopa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Neointimal Hyperplasia ◽  
Endothelial Injury ◽  
Collagen Content ◽  
Arterial Stenosis ◽  
Matrix Metalloproteinase 2 ◽  
Vessel Wall Thickness ◽  
Artery Disease

AbstractVascular restenosis remains a major problem in patients with coronary artery disease (CAD) and peripheral artery disease (PAD). Neointimal hyperplasia, defined by post-procedure proliferation and migration of vascular smooth muscle cells (VSMCs) is a key underlying pathology. Here we investigated the role of Interleukin 11 (IL-11) in a mouse model of injury-related plaque development. Apoe−/− mice were fed a hyperlipidaemic diet and subjected to carotid wire injury of the right carotid. Mice were injected with an anti-IL11 antibody (X203), IgG control antibody or buffer. We performed ultrasound analysis to assess vessel wall thickness and blood velocity. Using histology and immunofluorescence approaches, we determined the effects of IL-11 inhibition on VSMC and macrophages phenotypes and fibrosis. Treatment of mice with carotid wire injury using X203 significantly reduced post-endothelial injury vessel wall thickness, and injury-related plaque, when compared to control. Immunofluorescence staining of the injury-related plaque showed that X203 treatment did not reduce macrophage numbers, but reduced the number of VSMCs and lowered matrix metalloproteinase 2 (MMP2) levels and collagen content in comparison to control. X203 treatment was associated with a significant increase in smooth muscle protein 22α (SM22α) positive cells in injury-related plaque compared to control, suggesting preservation of the contractile VSMC phenotype. Interestingly, X203 also reduced the collagen content of uninjured carotid arteries as compared to IgG, showing an additional effect on hyperlipidemia-induced arterial remodeling in the absence of mechanical injury. Therapeutic inhibition of IL-11 reduced vessel wall thickness, attenuated neointimal hyperplasia, and has favorable effects on vascular remodeling following wire-induced endothelial injury. This suggests IL-11 inhibition as a potential novel therapeutic approach to reduce arterial stenosis following revascularization in CAD and PAD patients.

Atherosclerosis: Carotid vessel wall thickness and aortic stiffness compared to stenosis class in peripheral arterial disease

2013 ◽  
Vol 24 ◽  
pp. e38-e39
Author(s):  
Harrie CM van den Bosch ◽  
Jos JM Westenberg ◽  
Wikke Setz-Pels ◽  
Alette Daniels-Gooszen ◽  
Lucien EM Duijm ◽  
...  
Keyword(s):  
Peripheral Arterial Disease ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Aortic Stiffness ◽  
Arterial Disease ◽  
Vessel Wall Thickness ◽  
Carotid Vessel Wall ◽  
Peripheral Arterial ◽  
Carotid Vessel

Towards Non-Invasive Pressure Assessment

2010 ◽  
Author(s):  
Nathalie Bijnens ◽  
Bart Beulen ◽  
Peter Brands ◽  
Marcel Rutten ◽  
Frans van de Vosse
Keyword(s):  
Wall Thickness ◽  
Vessel Wall ◽  
Biomechanical Properties ◽  
Vessel Diameter ◽  
Local Pressure ◽  
Vessel Wall Thickness ◽  
Non Invasive ◽  
Vascular Impedance ◽  
Vessel Wall Properties ◽  
Invasive Techniques

In clinical practice, ultrasound is frequently applied to non-invasively assess blood velocity, blood volume flow and blood vessel wall properties such as vessel wall thickness and vessel diameter waveforms. To convert these properties into relevant biomechanical properties that are related to cardiovascular disease (CVD), such as elastic modulus and compliance of the vessel wall, local pressure has to be assessed simultaneously with vessel wall thickness and vessel diameter waveforms. Additionally, accurate estimates of vascular impedance (transfer function between pressure and blood flow) can be a valuable tool for the estimation of the condition of the vessel, e.g., to diagnose stenosis. Studies of arterial impedance in humans, however, are hampered by the lack of reliable non-invasive techniques to simultaneously record pressure and flow locally as a function of time. Local pressure assessment together with flow has great potential for improving the ability to diagnose and monitor CVD.

Human Carotid Atherosclerotic Plaque Growth Function and Progression Simulation Using Meshless GFD and Statistical Methods Based on Multi-Year In Vivo MRI

2008 ◽  
Author(s):  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Zhongzhao Teng ◽  
Chun Yuan ◽  
Gador Canton ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Plaque Rupture ◽  
Patient Specific ◽  
Tracking Data ◽  
Plaque Progression ◽  
Vessel Wall Thickness ◽  
Plaque Growth

Atherosclerotic plaque rupture and progression have been the focus of intensive investigations in recent years. The mechanisms governing plaque progression and rupture process are not well understood. Using computational models based on patient-specific multi-year in vivo MRI data, our recent results indicated that 18 out of 21 patients studied showed significant negative correlation between plaque progression measured by vessel wall thickness increase (WTI) and plaque wall (structural) stress (PWS) [1]. In this paper, a computational procedure based on meshless generalized finite difference (MGFD) method and serial magnetic resonance imaging (MRI) data was introduced to simulate plaque progression. Participating patients were scanned three times (T1, T2, and T3, at intervals of approximately 18 months) to obtain plaque progression data. Vessel wall thickness (WT) changes were used as the measure for plaque progression. Starting from T2 plaque geometry, plaque progression was simulated by solving the solid model and adjusting wall thickness using plaque growth functions iteratively until time T3 is reached. Numerically simulated plaque progression showed very good agreement with actual plaque geometry at T3 given by MRI data. We believe this is the first time plaque progression simulation results based on multi-year patient-tracking data are reported. Multi-year tracking data and MRI-based progression simulation add time dimension to plaque vulnerability assessment and will improve prediction accuracy.

scholarly journals Increased Coronary Vessel Wall Thickness in HIV-Infected Young Adults

2014 ◽  
Vol 59 (12) ◽  
pp. 1779-1786 ◽  
Author(s):  
K. Z. Abd-Elmoniem ◽  
A. B. Unsal ◽  
S. Eshera ◽  
J. R. Matta ◽  
N. Muldoon ◽  
...  
Keyword(s):  
Young Adults ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Coronary Vessel ◽  
Coronary Vessel Wall ◽  
Vessel Wall Thickness

Subvoxel vessel wall thickness measurements from vessel wall MR images

2019 ◽  
Author(s):  
K. M. van Hespen ◽  
Jaco J.M. Zwanenburg ◽  
J. Hendrikse ◽  
H. J. Kuijf
Keyword(s):  
Wall Thickness ◽  
Vessel Wall ◽  
Mr Images ◽  
Vessel Wall Thickness ◽  
Thickness Measurements

scholarly journals Human solCD39 inhibits injury-induced development of neointimal hyperplasia

2010 ◽  
Vol 103 (02) ◽  
pp. 426-435 ◽  
Author(s):  
Rosemary Kraemer ◽  
Hao Shen ◽  
Rita Upmacis ◽  
Aaron Marcus ◽  
Elgilda Musi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Platelet Activation ◽  
Blood Platelets ◽  
Neointimal Hyperplasia ◽  
Endothelial Injury ◽  
Vascular Endothelial ◽  
Leukocyte Infiltration ◽  
Post Injury ◽  
Arterial Lumen ◽  
Activated Platelets

SummaryBlood platelets provide the initial response to vascular endothelial injury, becoming activated as they adhere to the injured site. Activated platelets recruit leukocytes, and initiate proliferation and migration of vascular smooth muscle cells (SMC) within the injured vessel wall, leading to development of neointimal hyperplasia. Endothelial CD39/NTPDase1 and recombinant solCD39 rapidly metabolise nucleotides, including stimulatory ADP released from activated platelets, thereby suppressing additional platelet reactivity. Using a murine model of vascular endothelial injury, we investigated whether circulating human solCD39 could reduce platelet activation and accumulation, thus abating leukocyte infiltration and neointimal formation following vascular damage. Intraperitoneally-administered solCD39 ADP -ase activity in plasma peaked 1 hour (h) post-injection, with an elimination half-life of 43 h. Accordingly, mice were administered solCD39 or saline 1 h prior to vessel injury, then either sacrificed 24 h post-injury or treated with solCD39 or saline (three times weekly) for an additional 18 days. Twenty-four hours post-injury, solCD39-treated mice displayed a reduction in platelet activation and recruitment, P-selectin expression, and leukocyte accumulation in the arterial lumen. Furthermore, repeated administration of solCD39 modulated the late stage of vascular injury by suppressing leukocyte deposition, macrophage infiltration and smooth muscle cell (SMC) proliferation/migration, resulting in abrogation of neointimal thickening. In contrast, injured femoral arteries of saline-injected mice exhibited massive platelet thrombus formation, marked P-selectin expression, and leukocyte infiltration. Pronounced neointimal growth with macrophage and SMC accretion was also observed (intimal-to-medial area ratio 1.56 ± 0.34 at 19 days). Thus, systemic administration of solCD39 profoundly affects injury-induced cellular responses, minimising platelet deposition and leukocyte recruitment, and suppressing neointimal hyperplasia.

Abstract 2246: Coronary Arterial Positive Remodeling Detected by MRI: The Multi-Ethnic Study of Atherosclerosis (MESA)

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Cuilian Miao ◽  
Shaoguang Chen ◽  
Robson Macedo ◽  
Shenghan Lai ◽  
Kiang Liu ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Vessel Wall ◽  
Black Blood ◽  
Lumen Area ◽  
Outer Contour ◽  
Cross Sectional ◽  
Men And Women ◽  
Vessel Size ◽  
Vessel Wall Thickness ◽  
Before And After

The purpose of this study was to determine the ability of magnetic resonance imaging (MRI) to detect early changes of coronary atherosclerotic remodeling. Positive remodeling is associated with plaque vulnerability and rupture. 179 subjects (90 men, age 61±9 yrs) free of clinical cardiovascular disease underwent cross-sectional coronary wall MRI using a black blood technique. Outer contour area (“vessel size”), lumen area, and mean vessel wall thickness were obtained. Linear regression was used to determine the correlations of mean wall thickness with outer contour area or lumen area before and after adjustment for body size parameters. The outer contour area increased with increasing mean wall thickness (p<0.0001). Lumen area also increased, but at a smaller rate than outer contour area (p<0.0001). When men and women were examined separately (Figure ), the relationships continued to be significant (P<0.0001 and 0.05 respectively) with no differences in these relationships between men and women. When vessel size was normalized by LV size or body mass index, the relationships remained significant, and the relative slopes were similar to that in the non-normalized model. The positive correlations between outer contour area and vessel wall thickness remained significant for each coronary bed (right, left main, left anterior descending) individually.

Shear stress and the IVUS derived vessel wall thickness

2003 ◽  
pp. 148-164
Author(s):  
J. J. Wentzel ◽  
C. Cheng ◽  
R. de Crom ◽  
N. Stergiopulos ◽  
P. W. Serruys ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Vessel Wall Thickness

Abstract TP403: Sex-Dependent Differences in a Mouse Model of Acta2-Related Cerebrovascular Disease

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jamie M Wright ◽  
Jiyuan Chen ◽  
Dianna M Milewicz
Keyword(s):  
Cerebrovascular Disease ◽  
Wall Thickness ◽  
Vessel Wall ◽  
Vascular System ◽  
Smooth Muscle Actin ◽  
T Test ◽  
Missense Mutations ◽  
Male And Female ◽  
Vessel Wall Thickness ◽  
Significant Difference

Moyamoya Disease is two to four times more common in females than males. The underlying mechanisms behind this are currently unknown. Missense mutations in Acta2 predispose affected individuals to a variety of vascular diseases, including Moyamoya-like cerebrovascular disease. In this study we examined vessel wall thickness on H&E stained brain sections from WT and Acta2-/- male and female mice at 12 weeks of age (n=3 per a group). We found that female Acta2-/- mice had significantly greater percent vessel wall thickness compared to male Acta2-/- mice across all vessel sizes. There was not a significant difference between male and female vessel wall thickness in the wild-type groups. These findings in Acta2-/- mice suggest important sex-dependent differences in the function of α-smooth muscle actin (SMA) in the cerebrovascular system, and likely the vascular system as a whole. This has important implications for the design of studies examining the role of SMA in cerebrovascular disease and the investigation of novel therapies. Figure. Percent wall thickness (%TH) by sex. Two-tailed two-sample t-Test assuming unequal variances: * = p<0.05, ** = p<0.005, *** = p<0.0005 and # = one-tailed t-test significant but not two-tailed. SL=short vessel diameter.

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