ATP acts as a survival signal and prevents the mineralization of aortic valve

Côté, Nancy; Husseini, Diala El; Pépin, Andrée; Guauque-Olarte, Sandra; Ducharme, Valérie; Bouchard-Cannon, Pascale; Audet, Audrey; Fournier, Dominique; Gaudreault, Nathalie; Derbali, Habib; McKee, Marc D.; Simard, Chantale; Després, Jean‐Pierre; Pîbarot, Philippe; Bossé, Yohan; Mathieu, Patrick

doi:10.1016/j.yjmcc.2012.02.003

Cited by 84 publications

(53 citation statements)

References 35 publications

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“…217 Released ATP causes the survival of valvular interstitial cells in the aortic valve via P2Y 2 receptors and a high level of membrane-bound ectonucleotidase ecto-nucleotidase pyrophosphatase 1 is expressed in calcific aortic valve disease. Inhibition of ectonucleotidase with ARL67156 prevented the development of calcific aortic valve disease in warfarin-treated rats.…”

Section: Calcific Aortic Valve Diseasementioning

confidence: 99%

Purinergic Signaling in the Cardiovascular System

Burnstock

2017

Circulation Research

339

295

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Abstract:There is nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory-motor nerves, as well as in intracardiac neurons. Centers in the brain control heart activities and vagal cardiovascular reflexes involve purines. Adenine nucleotides and nucleosides act on purinoceptors on cardiomyocytes, AV and SA nodes, cardiac fibroblasts, and coronary blood vessels. Vascular tone is controlled by a dual mechanism. ATP, released from perivascular sympathetic nerves, causes vasoconstriction largely via P2X1 receptors. Endothelial cells release ATP in response to changes in blood flow (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostaglandins to cause vasodilation. ATP is also released from sensory-motor nerves during antidromic reflex activity, to produce relaxation of some blood vessels. Purinergic signaling is involved in the physiology of erythrocytes, platelets, and leukocytes. ATP is released from erythrocytes and platelets, and purinoceptors and ectonucleotidases are expressed by these cells. P1, P2Y 1 , P2Y 12 , and P2X1 receptors are expressed on platelets, which mediate platelet aggregation and shape change. Long-term (trophic) actions of purine and pyrimidine nucleosides and nucleotides promote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and P2Y receptors during angiogenesis, vessel remodeling during restenosis after angioplasty and atherosclerosis. The involvement of purinergic signaling in cardiovascular pathophysiology and its therapeutic potential are discussed, including heart failure, infarction, arrhythmias, syncope, cardiomyopathy, angina, heart transplantation and coronary bypass grafts, coronary artery disease, diabetic cardiomyopathy, hypertension, ischemia, thrombosis, diabetes mellitus, and migraine. (Circ Res. 2017;120:207-228.

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Section: Calcific Aortic Valve Diseasementioning

confidence: 99%

Purinergic Signaling in the Cardiovascular System

Burnstock

2017

Circulation Research

339

295

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“…ATP acts as a survival signal and prevents mineralization of aortic valve that occurs in calcific aortic valve disease (Osman et al, 2006;Côté et al, 2012b). Released ATP promoted the survival of valvular interstitial cells in the aortic valve via P2Y 2 receptors, and it was also shown that a high level of membranebound ectonucleotidase ENPP1 was expressed in calcific aortic valve disease.…”

Section: Calcific Aortic Valve Diseasementioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…Apoptosis/necrosis‐enabled dystrophic calcification mechanisms, in which cell injury is an important and early event, are exemplified by the failure of glutaraldehyde‐treated bioprosthetic substitute heart valves, in which calcification is initiated primarily within residual, non‐viable porcine aortic valve or bovine pericardial cells 14. Mineral found in CAVD is mostly hydroxyapatite of calcium (HAC), similar to bone mineral, which can be deposited by an apoptosis‐mediated process or by osteogenic activity 15, 16. In some explanted stenotic aortic valves (∼15%), well‐differentiated osseous metaplasia is present, suggesting that a process analogous to bone ossification may occur during the development of CAVD 17.…”

Section: Pathobiologymentioning

confidence: 99%

“…Pyrophosphate (PPi) is a powerful inhibitor of the nucleation of HAC whereas inorganic phosphate (Pi) has pro‐mineralising properties. Both NPP1 and ALP promote mineralisation during CAVD by elevating the Pi/PPi ratio 16, 21. In this regard, ALP, which is highly expressed during the mineralisation of VICs, transforms PPi into Pi 22.…”

Section: Pathobiologymentioning

confidence: 99%

The pathology and pathobiology of bicuspid aortic valve: State of the art and novel research perspectives

Mathieu

Bossé

Huggins

et al. 2015

The Journal of Pathology CR

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Bicuspid aortic valve is the most prevalent cardiac valvular malformation. It is associated with a high rate of long‐term morbidity including development of calcific aortic valve disease, aortic regurgitation and concomitant thoracic aortic aneurysm and dissection. Recently, basic and translational studies have identified some key processes involved in the development of bicuspid aortic valve and its morbidity. The development of aortic valve disease and thoracic aortic aneurysm and dissection is the result of complex interactions between genotypes, environmental risk factors and specific haemodynamic conditions created by bicuspid aortic valve anatomy. Herein, we review the pathobiology of bicuspid aortic valve with a special emphasis on translational aspects of these basic findings. Important but unresolved problems in the pathology of bicuspid aortic valve and thoracic aortic aneurysm and dissection are discussed, along with the molecular processes involved.

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ATP acts as a survival signal and prevents the mineralization of aortic valve

Cited by 84 publications

References 35 publications

Purinergic Signaling in the Cardiovascular System

Purinergic Signaling in the Cardiovascular System

Purinergic Signaling and Blood Vessels in Health and Disease

The pathology and pathobiology of bicuspid aortic valve: State of the art and novel research perspectives

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