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Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. Y., additional, Arvanitis, D. A., additional, Mourouzis, I., additional, Pantos, C., additional, Kranias, E. G., additional, Cokkinos, D. V., additional, Sanoudou, D., additional, Vladimirskaya, T. E., additional, Shved, I. A., additional, Kryvorot, S. G., additional, Schirmer, I. M., additional, Appukuttan, A., additional, Pott, L., additional, Jaquet, K., additional, Ladilov, Y., additional, Archer, C. R., additional, Bootman, M. D., additional, Roderick, H. L., additional, Fusco, A., additional, Sorriento, D., additional, Santulli, G., additional, Trimarco, B., additional, Iaccarino, G., additional, Hagenmueller, M., additional, Riffel, J., additional, Bernhold, E., additional, Katus, H. A., additional, Hardt, S. E., additional, Maqsood, A., additional, Zi, M., additional, Prehar, S., additional, Neyses, L., additional, Ray, S., additional, Oceandy, D., additional, Khatami, N., additional, Wadowski, P., additional, Wagh, V., additional, Hescheler, J., additional, Sachinidis, A., additional, Mohl, W., additional, Chaudhry, B., additional, Burns, D., additional, Henderson, D. J., additional, Bax, N. A. M., additional, Van Marion, M. H., additional, Shah, B., additional, Goumans, M. J., additional, Bouten, C. V. C., additional, Van Der Schaft, D. W. J., additional, Van Oorschot, A. A. M., additional, Maas, S., additional, Braun, J., additional, Van Tuyn, J., additional, De Vries, A. A. F., additional, Gittenberger-De Groot, A. C., additional, Bageghni, S., additional, Drinkhill, M. J., additional, Batten, T. F. C., additional, Ainscough, J. F. X., additional, Onate, B., additional, Vilahur, G., additional, Ferrer-Lorente, R., additional, Ybarra, J., additional, Diez-Caballero, A., additional, Ballesta-Lopez, C., additional, Moscatiello, F., additional, Herrero, J., additional, Badimon, L., additional, Martin-Rendon, E., additional, Clifford, D. M., additional, Fisher, S. A., additional, Brusnkill, S. J., additional, Doree, C., additional, Mathur, A., additional, Clarke, M., additional, Watt, S. M., additional, Hernandez-Vera, R., additional, Kavanagh, D., additional, Yemm, A. I., additional, Frampton, J., additional, Kalia, N., additional, Terajima, Y., additional, Shimizu, T., additional, Tsuruyama, S., additional, Ishii, H., additional, Sekine, H., additional, Hagiwara, N., additional, Okano, T., additional, Vrijsen, K. R., additional, Chamuleau, S. A. J., additional, Sluijter, J. P. G., additional, Doevendans, P. F. M., additional, Madonna, R., additional, Delli Pizzi, S., additional, Di Donato, L., additional, Mariotti, A., additional, Di Carlo, L., additional, D'ugo, E., additional, Teberino, M. A., additional, Merla, A., additional, T, A., additional, De Caterina, R., additional, Kolker, L., additional, Ali, N. N., additional, Maclellan, K., additional, Moore, M., additional, Wheeler, J., additional, Harding, S. E., additional, Fleck, R. A., additional, Rowlinson, J. M., additional, Kraenkel, N., additional, Ascione, R., additional, Madeddu, P., additional, O'sullivan, J. F., additional, Leblond, A. L., additional, Kelly, G., additional, Kumar, A. H. S., additional, Metharom, P., additional, Buneker, C. K., additional, Alizadeh-Vikali, N., additional, Hynes, B. G., additional, O'connor, R., additional, Caplice, N. M., additional, Noseda, M., additional, De Smith, A. J., additional, Leja, T., additional, Rao, P. H., additional, Al-Beidh, F., additional, Abreu Pavia, M. S., additional, Blakemore, A. I., additional, Schneider, M. D., additional, Stathopoulou, K., additional, Cuello, F., additional, Ehler, E., additional, Haworth, R. S., additional, Avkiran, M., additional, Morawietz, H., additional, Eickholt, C., additional, Langbein, H., additional, Brux, M., additional, Goettsch, C., additional, Goettsch, W., additional, Arsov, A., additional, Brunssen, C., additional, Mazilu, L., additional, Parepa, I. R., additional, Suceveanu, A. I., additional, Suceveanu, A. P., additional, De Man, F. S., additional, Guignabert, C., additional, Tu, L., additional, Handoko, M. L., additional, Schalij, I., additional, Fadel, E., additional, Postmus, P. E., additional, Vonk-Noordegraaf, A., additional, Humbert, M., additional, Eddahibi, S., additional, Del Giudice, C., additional, Anastasio, A., additional, Fazal, L., additional, Azibani, F., additional, Bihry, N., additional, Merval, R., additional, Polidano, E., additional, Samuel, J.-L., additional, Delcayre, C., additional, Zhang, Y., additional, Mi, Y. M., additional, Ren, L. L., additional, Cheng, Y. P., additional, Guo, R., additional, Liu, Y., additional, Jiang, Y. N., additional, Kokkinos, A. D., additional, Tretjakovs, P., additional, Jurka, A., additional, Bormane, I., additional, Mikelsone, I., additional, Reihmane, D., additional, Elksne, K., additional, Krievina, G., additional, Verbovenko, J., additional, Bahs, G., additional, Lopez-Andres, N., additional, Rousseau, A., additional, Calvier, L., additional, Akhtar, R., additional, Labat, C., additional, Cruickshank, K., additional, Diez, J., additional, Zannad, F., additional, Lacolley, P., additional, Rossignol, P., additional, Hamesch, K., additional, Subramanian, P., additional, Li, X., additional, Thiemann, A., additional, Heyll, K., additional, Dembowsky, K., additional, Chevalier, E., additional, Weber, C., additional, Schober, A., additional, Yang, L., additional, Kim, G., additional, Gardner, B., additional, Earley, J., additional, Hofmann-Bowman, M., additional, Cheng, C.-F., additional, Lian, W.-S., additional, Lin, H., additional, Jinjolia, N. J., additional, Abuladze, G. A., additional, Tvalchrelidze, S. H. T., additional, Khamnagadaev, I., additional, Shkolnikova, M., additional, Kokov, L., additional, Miklashevich, I., additional, Drozdov, I., additional, Ilyich, I., additional, Bingen, B. O., additional, Askar, S. F. A., additional, Ypey, D. L., additional, Van Der Laarse, A., additional, Schalij, M. J., additional, Pijnappels, D. A., additional, Roney, C. H., additional, Ng, F. S., additional, Chowdhury, R. A., additional, Chang, E. T. Y., additional, Patel, P. M., additional, Lyon, A. R., additional, Siggers, J. H., additional, Peters, N. S., additional, Obergrussberger, A., additional, Stoelzle, S., additional, Bruggemann, A., additional, Haarmann, C., additional, George, M., additional, Fertig, N., additional, Moreira, D., additional, Souza, A., additional, Valente, P., additional, Kornej, J., additional, Reihardt, C., additional, Kosiuk, J., additional, Arya, A., additional, Hindricks, G., additional, Adams, V., additional, Husser, D., additional, Bollmann, A., additional, Camelliti, P., additional, Dudhia, J., additional, Dias, P., additional, Cartledge, J., additional, Connolly, D. J., additional, Nobles, M., additional, Sebastian, S., additional, Tinker, A., additional, Opel, A., additional, Daimi, H., additional, Haj Khelil, A., additional, Be Chibani, J., additional, Barana, A., additional, Amoros, I., additional, Gonzalez De La Fuente, M., additional, Caballero, R., additional, Aranega, A., additional, Kelly, A., additional, Bernus, O., additional, Kemi, O. J., additional, Myles, R. C., additional, Ghouri, I. A., additional, Burton, F. L., additional, Smith, G. L., additional, Del Lungo, M., additional, Sartiani, L., additional, Spinelli, V., additional, Baruscotti, M., additional, Difrancesco, D., additional, Mugelli, A., additional, Cerbai, E., additional, Thomas, A. M., additional, Aziz, Q., additional, Khambra, T., additional, Addlestone, J. M. A., additional, Cartwright, E. J., additional, Wilkinson, R., additional, Song, W., additional, Marston, S., additional, Jacquet, A., additional, Mougenot, N. M., additional, Lipskaia, A. J., additional, Paalberends, E. R., additional, Stam, K., additional, Van Dijk, S. J., additional, Van Slegtenhorst, M., additional, Dos Remedios, C., additional, Ten Cate, F. J., additional, Michels, M., additional, Niessen, H. W. M., additional, Stienen, G. J. M., additional, Van Der Velden, J., additional, Read, M. I., additional, Andreianova, A. A., additional, Harrison, J. C., additional, Goulton, C. S., additional, Kerr, D. S., additional, Sammut, I. A., additional, Wallner, M., additional, Von Lewinski, D., additional, Kindsvater, D., additional, Saes, M., additional, Morano, I., additional, Muegge, A., additional, Buyandelger, B., additional, Kostin, S., additional, Gunkel, S., additional, Vouffo, J., additional, Ng, K., additional, Chen, J., additional, Eilers, M., additional, Isaacson, R., additional, Milting, H., additional, Knoell, R., additional, Cattin, M.-E., additional, Crocini, C., additional, Schlossarek, S., additional, Maron, S., additional, Hansen, A., additional, Eschenhagen, T., additional, Carrier, L., additional, Bonne, G., additional, Coppini, R., additional, Ferrantini, C., additional, Olivotto, I., additional, Belardinelli, L., additional, Poggesi, C., additional, Leung, M. C., additional, Messer, A. E., additional, Copeland, O., additional, Marston, S. B., additional, Mills, A. M., additional, Collins, T., additional, O'gara, P., additional, Thum, T., additional, Regalla, K., additional, Macleod, K. T., additional, Prodromakis, T., additional, Chaudhry, U., additional, Darzi, A., additional, Yacoub, M. H., additional, Athanasiou, T., additional, Bogdanova, A., additional, Makhro, A., additional, Hoydal, M., additional, Stolen, T. O., additional, Johnssen, A. B., additional, Alves, M., additional, Catalucci, D., additional, Condorelli, G., additional, Koch, L. G., additional, Britton, S. L., additional, Wisloff, U., additional, Bito, V., additional, Claus, P., additional, Vermeulen, K., additional, Huysmans, C., additional, Ventura-Clapier, R., additional, Sipido, K. R., additional, Seliuk, M. N., additional, Burlaka, A. P., additional, Sidorik, E. P., additional, Khaitovych, N. V., additional, Kozachok, M. M., additional, Potaskalova, V. S., additional, Driesen, R. B., additional, Galan, D. T., additional, De Paulis, D., additional, Arnoux, T., additional, Schaller, S., additional, Pruss, R. M., additional, Poitz, D. M., additional, Augstein, A., additional, Braun-Dullaeus, R. 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A., additional, Orban, K., additional, Murlasits, Z. S., additional, Balogh, L., additional, Varga, C., additional, Ku, H. C., additional, Su, M. J., additional, Chreih, R.-M., additional, Ginghina, C., additional, Deleanu, D., additional, Ferreira, A. L. B. J., additional, Belal, A., additional, Ali, M. A., additional, Fan, X., additional, Holt, A., additional, Campbell, R., additional, Schulz, R., additional, Bonanad, C., additional, Bodi, V., additional, Sanchis, J., additional, Morales, J. M., additional, Marrachelli, V., additional, Nunez, J., additional, Forteza, M. J., additional, Chaustre, F., additional, Gomez, C., additional, Chorro, F. J., additional, Csont, T., additional, Fekete, V., additional, Murlasits, Z., additional, Aypar, E., additional, Bencsik, P., additional, Sarkozy, M., additional, Varga, Z. V., additional, Ferdinandy, P., additional, Duerr, G. 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Published
2012
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9. Mechanical properties and structure of carotid arteries in mice lacking desmin

Author

Lacolley, Patrick, Challande, Pascal, Boumaza, Saliha, Cohuet, Géraldine, Laurent, Stéphane, Boutouyrie, Pierre, Grimaud, Jean-Alexis, Paulin, Denise, Lamazière, Jean-Marie Daniel, and Li, Zhenlin

Abstract

Objective: Our aim was to determine in desmin homozygous mutant mice the viscoelastic properties, the mechanical strength and the structure of the carotid artery. Methods: To assess the viscoelastic properties of large arteries, we have performed an in vivo analysis of the diameter–, and distensibility–pressure curves of the common carotid artery (CCA) in homozygous (Des –/–), heterozygous (Des +/–) and wild-type (Des +/+) mice. To evaluate the mechanical strength, we have measured the in vitro intraluminal pressure producing the rupture of the carotid artery wall. The structure analysis of the arterial wall was based on histology and electronic microscopy. Results: A lower distensibility and an increase of arterial wall viscosity were observed in Des –/– compared with Des +/+. Arterial thickness of Des –/– was similar to those of Des +/+, without changes in elastin and collagen contents. Electron microscopy revealed that the perimeter of cellular fingerlike-projections was smaller in Des –/–, indicating that the cells have lost part of their connections to the extracellular matrix. The rupture pressure was significantly lower in Des –/– (1500±200 mmHg) compared with Des +/+ (2100±80 mmHg) indicating a lower mechanical strength of the vascular wall. No significant difference was found between Des +/– and Des +/+. Conclusion: The desmin is essential to maintain proper viscoelastic properties, structure and mechanical strength of the vascular wall.

Published
2001
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10. The VWF/LRP4/αVβ3-axis represents a novel pathway regulating proliferation of human vascular smooth muscle cells.

Author

Lagrange J, Worou ME, Michel JB, Raoul A, Didelot M, Muczynski V, Legendre P, Plénat F, Gauchotte G, Lourenco-Rodrigues MD, Christophe OD, Lenting PJ, Lacolley P, Denis CV, and Regnault V

Subjects
Animals, Atherosclerosis genetics, Atherosclerosis pathology, Carotid Artery Injuries genetics, Carotid Artery Injuries metabolism, Carotid Artery Injuries pathology, Cell Movement, Cells, Cultured, Hyperplasia, Integrin alphaVbeta3 genetics, LDL-Receptor Related Proteins genetics, Male, Mice, Inbred C57BL, Mice, Knockout, Muscle, Smooth, Vascular injuries, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle pathology, Neointima, Plaque, Atherosclerotic, Signal Transduction, Vascular System Injuries genetics, Vascular System Injuries metabolism, Vascular System Injuries pathology, von Willebrand Factor genetics, Mice, Atherosclerosis metabolism, Cell Proliferation, Integrin alphaVbeta3 metabolism, LDL-Receptor Related Proteins metabolism, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, von Willebrand Factor metabolism
Abstract

Aims: Von Willebrand factor (VWF) is a plasma glycoprotein involved in primary haemostasis, while also having additional roles beyond haemostasis namely in cancer, inflammation, angiogenesis, and potentially in vascular smooth muscle cell (VSMC) proliferation. Here, we addressed how VWF modulates VSMC proliferation and investigated the underlying molecular pathways and the in vivo pathophysiological relevance., Methods and Results: VWF induced proliferation of human aortic VSMCs and also promoted VSMC migration. Treatment of cells with a siRNA against αv integrin or the RGT-peptide blocking αvβ3 signalling abolished proliferation. However, VWF did not bind to αvβ3 on VSMCs through its RGD-motif. Rather, we identified the VWF A2 domain as the region mediating binding to the cells. We hypothesized the involvement of a member of the LDL-related receptor protein (LRP) family due to their known ability to act as co-receptors. Using the universal LRP-inhibitor receptor-associated protein, we confirmed LRP-mediated VSMC proliferation. siRNA experiments and confocal fluorescence microscopy identified LRP4 as the VWF-counterreceptor on VSMCs. Also co-localization between αvβ3 and LRP4 was observed via proximity ligation analysis and immuno-precipitation experiments. The pathophysiological relevance of our data was supported by VWF-deficient mice having significantly reduced hyperplasia in carotid artery ligation and artery femoral denudation models. In wild-type mice, infiltration of VWF in intimal regions enriched in proliferating VSMCs was found. Interestingly, also analysis of human atherosclerotic lesions showed abundant VWF accumulation in VSMC-proliferating rich intimal areas., Conclusion: VWF mediates VSMC proliferation through a mechanism involving A2 domain binding to the LRP4 receptor and integrin αvβ3 signalling. Our findings provide new insights into the mechanisms that drive physiological repair and pathological hyperplasia of the arterial vessel wall. In addition, the VWF/LRP4-axis may represent a novel therapeutic target to modulate VSMC proliferation., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)

Published
2022
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11. Cell senescence: basic mechanisms and the need for computational networks in vascular ageing.

Author

Regnault V, Challande P, Pinet F, Li Z, and Lacolley P

Subjects
Animals, Blood Vessels metabolism, Cell Cycle Checkpoints, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Gene Expression Regulation, Gene Regulatory Networks, Humans, Protein Interaction Maps, Signal Transduction, Systems Biology, Vascular Diseases genetics, Vascular Diseases metabolism, Algorithms, Blood Vessels pathology, Cell Proliferation, Cellular Senescence, Computational Biology, Proteomics, Vascular Diseases pathology
Abstract

This review seeks to provide an update of the mechanisms of vascular cell senescence, from newly identified molecules to arterial ageing phenotypes, and finally to present a computational approach to connect these selected proteins in biological networks. We will discuss current key signalling and gene expression pathways by which these focus proteins and networks drive normal and accelerated vascular ageing. We also review the possibility that senolytic drugs, designed to restore normal cell differentiation and function, could effectively treat multiple age-related vascular diseases. Finally, we discuss how cell senescence is both a cause and a consequence of vascular ageing because of the possible feedback controls between identified networks., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)

Published
2021
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12. Smooth muscle cell and arterial aging: basic and clinical aspects.

Author

Lacolley P, Regnault V, and Avolio AP

Subjects
Age Factors, Aging metabolism, Animals, Arteries metabolism, Arteries physiopathology, Cell Differentiation, Cell Plasticity, Hemodynamics, Humans, Mechanotransduction, Cellular, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular physiopathology, Myocytes, Smooth Muscle metabolism, Phenotype, Vascular Stiffness, Aging pathology, Arteries pathology, Cellular Senescence, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle pathology
Abstract

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.

Published
2018
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15. Cyclic stretch-induced thrombin generation by rat vascular smooth muscle cells is mediated by the integrin αvβ3 pathway.

Author

Mao X, Said R, Louis H, Max JP, Bourhim M, Challande P, Wahl D, Li Z, Regnault V, and Lacolley P

Subjects
Animals, Aorta metabolism, Cell Survival, Cells, Cultured, Dose-Response Relationship, Drug, Integrin alphaVbeta3 antagonists & inhibitors, Integrin alphaVbeta3 genetics, Muscle, Smooth, Vascular drug effects, Myocytes, Smooth Muscle drug effects, Peptides, Cyclic pharmacology, Phosphorylation, Prothrombin metabolism, Pulsatile Flow, RNA Interference, Rats, Rats, Wistar, Stress, Mechanical, Talin genetics, Talin metabolism, Time Factors, Transfection, Up-Regulation, src-Family Kinases metabolism, Integrin alphaVbeta3 metabolism, Mechanotransduction, Cellular drug effects, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, Thrombin metabolism
Abstract

Aims: Vascular smooth muscle cell (VSMC) phenotypic modulation plays a pivotal role in atherothrombotic diseases. Thrombin generation at the surface of VSMCs and activation of integrin mechanotransduction pathways represent potential mechanisms. Here, we examine whether mechanical stretch increases thrombin generation on cultured rat aortic VSMCs., Methods and Results: The integrin α(v)β(3) antagonist peptide (cRGDPV) dose-dependently decreased thrombin generation without stretch. Static stretch (5%, 1 Hz) failed to modify the thrombin-forming capacity of VSMCs, whereas 10% cyclic stretch during 60 and 360 min enhanced integrin α(v)β(3) expression and thrombin generation at the surface of VSMCs by 30% without inducing apoptosis. Cyclic stretch also stimulated Src phosphorylation, cleavage of talin, and binding of prothrombin to VSMCs. Upregulation of α(v)β(3) expression, Src phosphorylation, and enhanced thrombin generation by cyclic stretch were abolished by cRGDPV and silencing RNA (siRNA) against α(v) as well as by selective inhibition of integrin α(v)β(3) inside-out signalling by a talin-siRNA. Complete abolition of stretch-induced VSMC-supported thrombin generation by the RGT peptide, which disrupts the interaction of Src with the β(3) cytoplasmic tail, demonstrates the link between outside-in pathways involving β(3)-Src interaction and thrombin activity dependent on inside-out signalling., Conclusion: These data show that the contribution of cyclic stretch to VSMC-supported thrombin generation is driven by the integrin α(v)β(3) signalling pathway and suggest a role for pulsatility-induced intramural thrombin in VSMC-dependent vascular remodelling.

Published
2012
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16. Genetics and pathophysiology of arterial stiffness.

Author

Lacolley P, Challande P, Osborne-Pellegrin M, and Regnault V

Subjects
Animals, Elasticity, Gene Expression Profiling, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Genetic, Pulsatile Flow, Regional Blood Flow, Risk Factors, Arteries physiopathology, Hemodynamics, Vascular Diseases genetics, Vascular Diseases physiopathology
Abstract

Arterial stiffness is a cardiovascular risk factor that is independent of arterial pressure. Clinically, carotid-femoral pulse wave velocity (PWV) is the gold-standard parameter of arterial stiffness. Recent genetic studies have revealed specific genes that contribute to arterial stiffening. Here we review the recent findings on genome-wide linkage analyses and candidate gene polymorphism association studies. We also focus on the latest advances in the identification of gene variants affecting PWV using high density array single nucleotide polymorphism technology in a recent genome-wide association (GWA) study. Linkage and polymorphism studies revealed a first group of genes affecting the renin-angiotensin-aldosterone system, elastic fibre structural components, metalloproteinases, and the NO pathway. A second group of genes, identified by polymorphism association studies and possibly involved in the pathophysiology of arterial stiffness, includes beta-adrenergic receptors, endothelin receptors, and inflammatory molecules. The last group of genes, identified by GWA studies and unrelated to currently suspected mechanisms of arterial stiffness, may target transcriptional pathways controlling gene expression, differentiation of vascular smooth muscle cells, apoptosis of endothelial cells, or the immune response within the vascular wall.

Published
2009
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17. Carotid arterial stiffness, elastic fibre network and vasoreactivity in semicarbazide-sensitive amine-oxidase null mouse.

Author

Mercier N, Osborne-Pellegrin M, El Hadri K, Kakou A, Labat C, Loufrani L, Henrion D, Challande P, Jalkanen S, Fève B, and Lacolley P

Subjects
Amine Oxidase (Copper-Containing) metabolism, Animals, Aorta, Blotting, Western methods, Carotid Artery, Common metabolism, Carotid Artery, Common pathology, Collagen analysis, Elastic Tissue metabolism, Elastic Tissue pathology, Elasticity, Elastin analysis, Immunoenzyme Techniques, In Vitro Techniques, Male, Mesenteric Arteries metabolism, Mesenteric Arteries pathology, Mesenteric Arteries physiology, Mice, Mice, Knockout, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Protein-Lysine 6-Oxidase analysis, Shear Strength, Vasomotor System physiology, Amine Oxidase (Copper-Containing) genetics, Carotid Artery, Common physiology, Elastic Tissue physiology, Muscle, Smooth, Vascular physiology
Abstract

Objective: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO -/-) using various techniques including high resolution echotracking., Methods and Results: SSAO -/- mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO -/- than in SSAO +/+ animals. Elastic modulus-wall stress curves and CA rupture pressure were similar between SSAO -/- and +/+ mice, indicating no change in arterial wall stiffness or mechanical strength. There was no significant difference in insoluble elastin, total collagen content and elastic lamellar morphology between the two genotypes. No alteration in vascular reactivity was observed in aortic rings and mesenteric arteries from SSAO -/- mice. Aortic lysyl oxidase (LO) activity remained unaltered, indicating that SSAO invalidation is not accompanied by a compensatory increase in LO activity., Conclusion: This is the first functional study of arteries lacking SSAO. Our results indicate that SSAO -/- mice present an increased arterial diameter associated with normal arterial mechanical properties, suggesting that SSAO deficiency might contribute to arterial wall remodeling. However, these results argue against the hypothesis that SSAO intervenes in elastic fibre organization, elastin cross-linking processes and vasoreactivity.

Published
2006
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