Vascular biomechanical properties in mice with smooth muscle specific deletion of Ndst1

Adhikari, Neeta; Billaud, Marie; Carlson, Marjorie; Lake, Spencer P.; Montaniel, Kim Ramil C.; Staggs, Rod; Guan, Weihua; Walek, Dinesha; Desir, Snider; Isakson, Brant E.; Barocas, Victor H.; Hall, Jennifer L.

doi:10.1007/s11010-013-1831-3

Cited by 4 publications

(1 citation statement)

References 79 publications

(100 reference statements)

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“…Indeed, Ndst1 conditional knockout mice show severe developmental defects in forebrain, eyes, as well as axon guidance errors (43). Also, in mice, targeted ablation of Ndst1 in smooth muscle cells resulted in altered expression of actin and myosin leading to arterial stiffness, which is a risk factor for cardiovascular disease (44).…”

Section: B the Anabolic Branch: Encoding Biological Function Throughmentioning

confidence: 99%

Syndecan Heparan Sulfate Proteoglycans: Regulation, Signaling and Impact on Tumor Biology

Gomes

Sinkevičiūtė

Multhaupt

et al. 2016

TIGG

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Virtually all animal cells express heparan sulfate proteoglycans on the cell surface and in the extracellular matrix. Syndecans are a major group of transmembrane proteoglycans functioning as receptors that mediate signal transmission from the extracellular microenvironment to the cell. Their heparan sulfate chains, due to their vast structural diversity, interact with a wide array of ligands including potent regulators of adhesion, migration, growth and survival. Frequently, ligands interact with cell surface heparan sulfate in conjunction with high affinity receptors. The consequent signaling can therefore be complex, but it is now known that syndecans are capable of independent signaling. This review is divided in two sections, and will first discuss how the assembly of heparan sulfate, the anabolic process, encodes information related to ligand binding and signaling. Second, we discuss how, in partial catabolic processes, new roles for HSPGs emerge that affect cell behavior. Examples from tumor studies are emphasized, since HSPGs may be altered in composition and distribution and may also represent targets for the development of new therapeutics.

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Section: B the Anabolic Branch: Encoding Biological Function Throughmentioning

confidence: 99%

Syndecan Heparan Sulfate Proteoglycans: Regulation, Signaling and Impact on Tumor Biology

Gomes

Sinkevičiūtė

Multhaupt

et al. 2016

TIGG

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Smooth muscle cell and arterial aging: basic and clinical aspects

Lacolley

Régnault

Avolio

2018

Cardiovascular Research

171

117

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Arterial aging engages a plethora of key signalling pathways that act in concert to induce vascular smooth muscle cell (VSMC) phenotypic changes leading to vascular degeneration and extracellular matrix degradation responsible for alterations of the mechanical properties of the vascular wall. This review highlights proof-of-concept examples of components of the extracellular matrix, VSMC receptors which connect extracellular and intracellular structures, and signalling pathways regulating changes in mechanotransduction and vascular homeostasis in aging. Furthermore, it provides a new framework for understanding how VSMC stiffness and adhesion to extracellular matrix contribute to arterial stiffness and how interactions with endothelial cells, platelets, and immune cells can regulate vascular aging. The identification of the key players of VSMC changes operating in large and small-sized arteries in response to increased mechanical load may be useful to better elucidate the causes and consequences of vascular aging and associated progression of hypertension, arteriosclerosis, and atherosclerosis.

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Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease

Lacolley

Régnault

Segers

et al. 2017

Physiological Reviews

550

417

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The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.

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Vascular biomechanical properties in mice with smooth muscle specific deletion of Ndst1

Cited by 4 publications

References 79 publications

Syndecan Heparan Sulfate Proteoglycans: Regulation, Signaling and Impact on Tumor Biology

Syndecan Heparan Sulfate Proteoglycans: Regulation, Signaling and Impact on Tumor Biology

Smooth muscle cell and arterial aging: basic and clinical aspects

Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease

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