Animal Models for Studies of Arterial Stiffness

Lacolley, Patrick; Thornton, Simon N.; Bézie, Yvonnick

doi:10.1007/978-1-4471-5198-2_6

Cited by 3 publications

(1 citation statement)

References 59 publications

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“…Several studies have reported the prognostic value of arterial stiffness in patient-and general populationbased cohorts as an independent predictor of cardiovascular events, morbidity, and all-cause mortality (Palombo and Kozakova, 2016). In line with these epidemiological findings, animal models of arterial stiffness associated with ECM remodelling have revealed fatal cardiovascular diseases and complications such as ischemia, aneurysms, and atherosclerosis (Kothapalli et al, 2012;Lacolley et al, 2014). We show here that depletion of arterial macrophages in healthy aorta led to reduced contractile function and increased aortic stiffness and collagen production.…”

Section: Discussionmentioning

confidence: 89%

Hyaluronan Receptor LYVE-1-Expressing Macrophages Maintain Arterial Tone through Hyaluronan-Mediated Regulation of Smooth Muscle Cell Collagen

et al. 2018

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The maintenance of appropriate arterial tone is critically important for normal physiological arterial function. However, the cellular and molecular mechanisms remain poorly defined. Here, we have shown that in the mouse aorta, resident macrophages prevented arterial stiffness and collagen deposition in the steady state. Using phenotyping, transcriptional profiling, and targeted deletion of Csf1r, we have demonstrated that these macrophages-which are a feature of blood vessels invested with smooth muscle cells (SMCs) in both mouse and human tissues-expressed the hyaluronan (HA) receptor LYVE-l. Furthermore, we have shown they possessed the unique ability to modulate collagen expression in SMCs by matrix metalloproteinase MMP-9-dependent proteolysis through engagement of LYVE-1 with the HA pericellular matrix of SMCs. Our study has unveiled a hitherto unknown homeostatic contribution of arterial LYVE-1 macrophages through the control of collagen production by SMCs and has identified a function of LYVE-1 in leukocytes.

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Section: Discussionmentioning

confidence: 89%

Hyaluronan Receptor LYVE-1-Expressing Macrophages Maintain Arterial Tone through Hyaluronan-Mediated Regulation of Smooth Muscle Cell Collagen

et al. 2018

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Pulse Wave Velocity and Prognosis in End-Stage Kidney Disease

Tripepi

Agharazii

Pannier³

et al. 2018

Hypertension

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High pulse wave velocity (PWV) is a hallmark of end-stage kidney disease (ESKD) where it is considered useful for risk stratification. We investigated whether PWV adds meaningful prognostic information to 2 simple, well-validated, clinical risk scores specific to ESKD (the Annualized Rate of Occurrence scores) for predicting all-cause and cardiovascular mortality by applying state-of-the-art prognostic tests including discrimination (Harrell C-index), risk reclassification (integrated discrimination improvement), and calibration. We performed these analyses in the 2 largest ESKD cohorts with available PWV data, the Manhes-Hospital cohort in Paris (n=287 patients) and the Quebec Research Center cohort in Canada (n=246 patients). The Harrell C-index of the 2 clinical risk scores was consistently higher than that by PWV both for all-cause (Manhes cohort, 77.5% versus 73.7%; Quebec cohort, 61.5% versus 58.9%) and cardiovascular mortality (Manhes cohort, 77.9% versus 77.2%; Quebec cohort, 63.8% versus 60.3%). Furthermore, PWV provided a very modest increase in discriminatory power over and above clinical risk scores by Harrell C-index (from 0.5% to 1.8%) and in risk reclassification by Integrated Discrimination Improvement (from 0.9% to 5.1%) and actually worsened models calibration. In patients with ESKD, PWV has a prognostic power for all-cause and cardiovascular mortality inferior to that by simple clinical risk scores and only modestly improves the risk discrimination and reclassification by the same risk scores and worsens models calibration. Clinicians may better rely on available clinical risk scores rather than on PWV for risk stratification in the ESKD population.

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Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action

Zhu

et al. 2019

Front. Physiol.

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Vascular smooth muscle cells (VSMCs) are the predominant cell type in the arterial wall. These cells play a critical role in maintaining vascular homeostasis including vasoconstriction and vasodilatation through active contraction and relaxation. Dysregulation of VSMC function alters the response of blood vessels to mechanical stress, contributing to the pathogenesis of vascular diseases, particularly atherosclerosis and hypertension. The stiffness of VSMCs is a major regulator of vascular function. Previous studies suggest that intracellular Ca 2+ controls the stiffness of VSMCs by a mechanism involving myosin contractile apparatus. More recent studies highlight important functions of cytoskeletal α-smooth muscle actin (α-SMA), α5β1 integrin, and integrin-mediated cell-extracellular matrix (ECM) interactions in Ca 2+ -dependent regulation of VSMC stiffness and adhesion to the ECM, providing novel insights into the mechanism of calcium action.

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Animal Models for Studies of Arterial Stiffness

Cited by 3 publications

References 59 publications

Hyaluronan Receptor LYVE-1-Expressing Macrophages Maintain Arterial Tone through Hyaluronan-Mediated Regulation of Smooth Muscle Cell Collagen

Hyaluronan Receptor LYVE-1-Expressing Macrophages Maintain Arterial Tone through Hyaluronan-Mediated Regulation of Smooth Muscle Cell Collagen

Pulse Wave Velocity and Prognosis in End-Stage Kidney Disease

Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action

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