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Books on the topic 'Vascular smooth muscle cell'

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Published: 4 June 2021

Last updated: 11 March 2023

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1

Karsten, Schrör, and Ney Peter 1930-, eds. Prostaglandins and control of vascular smooth muscle cell proliferation. Basel, Switzerland ; Boston, Mass: Birkhäuser Verlag, 1997.

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2

Schrör, Karsten, and Peter Ney, eds. Prostaglandins and Control of Vascular Smooth Muscle Cell Proliferation. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-7352-9.

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3

M, Schwartz Stephen, and Mecham Robert P, eds. The vascular smooth muscle cell: Molecular and biological responses to the extracellular matrix. San Diego: Academic Press, 1995.

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4

Leung, Wesley D. The role of apolipoprotein D in vascular smooth muscle cell migration. Ottawa: National Library of Canada, 2002.

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5

Sarjeant, Jennifer Mary. The role of apolipoprotein D in vascular smooth muscle cell proliferation. Ottawa: National Library of Canada, 2002.

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6

rdh-Nilsson, Anna Hultga. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. Stockholm: Kongl. Carolinska Medico Chirurgiska Institutet, 1991.

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7

Mitchell, Lylieth Paula-Ann. Vascular endothelial and smooth muscle cell apoptosis in vivo and in vitro. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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8

1930-, Sperelakis Nick, and Kuriyama Hiroshi 1928-, eds. Ion channels of vascular smooth muscle cells and endothelial cells: Proceedings of the International Society for Heart Research (ISHR), held in Cincinnati, Ohio, May 28 through June 2, 1991. New York: Elsevier, 1991.

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9

Perlmutter, Robin Alexandra. Differential effects of platelet-derived growth factor isoforms on large and small vessel endothelial cells and vascular smooth muscle cells. [s.l: s.n.], 1992.

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10

1946-, Bruschi G., and Borghetti Alberico, eds. Cellular aspects of hypertension. Berlin: Springer-Verlag, 1991.

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11

Gao, Yuansheng. Biology of Vascular Smooth Muscle. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7122-8.

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12

H, Campbell Julie, and Campbell Gordon R, eds. Vascular smooth muscle in culture. Boca Raton, Fla: CRC Press, 1987.

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13

K, Singal Pawan, Panagia Vincenzo, and Pierce Grant N, eds. The cellular basis of cardiovascular function in health and disease. Dordrecht: Kluwer Academic Publishers, 1997.

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14

J, Garland C., and Angus James A, eds. The pharmacology of vascular smooth muscle. Oxford: Oxford University Press, 1996.

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15

Ionic channels in vascular smooth muscle. Austin: R.G. Landes Co., 1994.

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16

C, Claycomb William, Di Nardo Paolo, and New York Academy of Sciences., eds. Cardiac growth and regeneration. New York, N.Y: New York Academy of Sciences, 1995.

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17

Gao, Yuansheng. Biology of Vascular Smooth Muscle: Vasoconstriction and Dilatation. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4810-4.

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18

International, Symposium on Vascular Neuroeffector Mechanisms (6th 1987 Melbourne Australia). Vascular neuroeffector mechanisms: Receptors, ion-channels, second messengers and endogenous mediators. Oxford: IRL Press, 1988.

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19

M, Vanhoutte Paul, Shepherd John T. 1919-, International Union of Physiological Sciences. Congress, and International Symposium on Mechanisms of Vasodilatation (4th : 1986 : Rochester, Minn.), eds. Vasodilatation: Vascular smooth muscle, peptides, autonomic nerves, and endothelium. New York: Raven Press, 1988.

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20

V, Cherni͡a︡vskai͡a︡ G., and Akademii͡a︡ nauk SSSR Biblioteka, eds. Gladkie mysht͡s︡y krovenosnykh sosudov: Bibliograficheskiĭ ukazatelʹ stateĭ : po materialam inostrannykh istochnikov, 1984-1988. Leningrad: BAN, 1989.

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21

Shuba, M. F. Fiziologii͡a︡ sosudistykh gladkikh mysht͡s︡. Kiev: Nauk. dumka, 1988.

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22

White, Pamela J. The role of P2Y receptors in human vascular smooth muscle. Leicester: De Montfort University, 2005.

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23

Statham, Fiona Kate. The regulation of protein kinase C activity in vascular smooth muscle. Manchester: University of Manchester, 1996.

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24

1942-, Sowers James R., ed. Endocrinology of the vasculature. Totowa, N.J: Humana Press, 1996.

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25

Hamel, Kenneth Carl. The role of activin in aortic smooth muscle cell growth. Ottawa: National Library of Canada, 1993.

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26

Advanced School on "Biomechanics of Soft Tissue" (2001 Udine, Italy). Biomechanics of soft tissue in cardiovascular systems. Wien: Springer, 2003.

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27

1930-, Bevan John A., ed. Vascular neuroeffector mechanisms: Proceedings of the Fifth International Congress on Vascular Neuroeffector Mechanisms held in Paris, France, on 6-8 August 1984. Amsterdam: Elsevier, 1985.

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28

International Symposium on Endothelium-Derived Hyperpolarizing Factor (2nd 1998 Cernay-la-Ville, France). Endothelium-dependent hyperpolarizations. Amsterdam: Harwood Academic, 1999.

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29

Hultgardh-Nilsson, Anna. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. [S.l: s.n.], 1991.

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30

Kirkup, Anthony Joseph. Modulation of membrane currents and mechanical activity by noradrenaline and other agents in vascular smooth muscle. Manchester: University of Manchester, 1995.

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31

Ibbotson, Timothy. The imidazoline/guanidine receptor site and its role in potassium channel moulation in vascular smooth muscle. Manchester: University of Manchester, 1993.

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32

The Vascular Smooth Muscle Cell. Elsevier, 1995. http://dx.doi.org/10.1016/b978-0-12-632310-8.x5000-1.

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33

Bochaton-Piallat, Marie-Luce, Carlie J. M. de Vries, and Guillaume J. van Eys. Vascular smooth muscle cells. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0007.

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To understand the function of arteries in the regulation of blood supply throughout the body it is essential to realize that the vessel wall is composed predominantly of smooth muscle cells (SMCs) with only one single layer of luminal endothelial cells. SMCs determine the structure of arteries and are decisive in the regulation of blood flow. This review describes the reason for the large variation of SMCs throughout the vascular tree. This depends on embryonic origin and local conditions. SMCs have the unique capacity to react to these conditions by modulating their phenotype. So, in one situation SMCs may be contractile in response to blood pressure, in another situation they may be synthetic, providing compounds to increase the strength of the vascular wall by reinforcing the extracellular matrix. This phenotypic plasticity is necessary to keep arteries functional in fulfilling the metabolic demands in the various tissues of the body.

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34

Nev, P., and K. Schrör. Prostaglandins and Control of Vascular Smooth Muscle Cell Proliferation. Springer Basel AG, 2012.

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35

Schwartz, Stephen M., and Robert P. Mecham. Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix. Elsevier Science & Technology Books, 1995.

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36

Schwartz, Stephen M. The Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1995.

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37

The Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1995.

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38

Song, Ping, Xiaoyan Dai, Qilong Wang, and Vicky E. MacRae, eds. Vascular Smooth Muscle Cell fate and Vascular Remodeling: Mechanisms, Therapeutic Targets, and Drugs, Volume I. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-070-5.

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39

Ho, Bernard. Integrin-linked kinase in the vascular smooth muscle cell response to arterial injury. 2006.

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40

Bolzon, Bradley John. Identification of the major ionic currents in vascular smooth muscle cells. 1992.

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41

Fleming, Ingrid, Brenda R. Kwak, and Merlijn J. Meens. The endothelial cell. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0006.

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The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.

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42

Michael, Piper Hans, ed. Cell culture technique in heart and vessel research. Berlin: Springer-Verlag, 1990.

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43

Merklinger, Sandra Lea. Progression and regression of pulmonary vascular disease related to smooth muscle cell apoptosis, S100A4/Mts1 and fibulin-5. 2005.

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44

Bolzon, Bradley J. *. The isolation and characterization of single vascular smooth muscle cells from spontaneously hypertensive rats. 1988.

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45

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.

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46

Declerck, I. Modulation of the Ca2+ Movements in Vascular Smooth Muscle Cells by the Co-Transmitters Noradrenaline and ATP. Leuven University Press, 1991.

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47

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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48

Sperelakis, Nicholas. Ion Channels of Vascular Smooth Muscle Cells and Endothelial Cells: Proceedings of the International Society for Heart Research (Ishr Held in Cinci). Elsevier Science Ltd, 1991.

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49

Hai, Chi-Ming. Vascular Smooth Muscle. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/10141.

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50

Peter Judith Ed. Judith Ed. Campbell. Vascular Smooth Muscle. CRC Press, 1987.

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