Relevant bibliographies by topics / Arterial Smooth Muscle Cell

Academic literature on the topic 'Arterial Smooth Muscle Cell'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Arterial Smooth Muscle Cell.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Arterial Smooth Muscle Cell"

1

Hao, Hiroyuki, Giulio Gabbiani, and Marie-Luce Bochaton-Piallat. "Arterial Smooth Muscle Cell Heterogeneity." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 9 (September 2003): 1510–20. http://dx.doi.org/10.1161/01.atv.0000090130.85752.ed.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Reidy, Michael A., and Christopher L. Jackson. "Factors Controlling Growth of Arterial Cells following Injury*." Toxicologic Pathology 18, no. 4a (January 1990): 547–53. http://dx.doi.org/10.1177/019262339001804a04.

Full text
Abstract:
The proliferation of vascular smooth muscle cells is a key event in the development of arterial lesions. In experimental models, loss of arterial endothelium followed by platelet adherence does not necessarily stimulate smooth muscle cell proliferation. Furthermore, using animals deficient in platelets, smooth muscle cell proliferation was induced to an equal extent as in control animals following injury with a balloon catheter. Modulation of the smooth muscle response, however, was achieved by totally denuding arteries with a technique which did not traumatize medial cells. These data suggested that injury and cell death might induce proliferation of cells by release of endogenous mitogen. Basic FGF is present in the arterial wall and addition of this mitogen to denuded arteries was found to cause a highly significant increase in smooth muscle cell proliferation. These studies suggest that smooth muscle cell proliferation could be induced by factors present in the arterial wall and does not require exogenous factors. Smooth muscle cell proliferation following balloon catheter injury is significantly reduced by administration of calcium antagonists. Repeated administration of nifedipine caused a significant reduction in intimal lesion size induced by injury. The anti-proliferative. effect was not observed in other tissues. Influx of Ca++ ions into medial smooth muscle cells may therefore be an obligatory step for replication.
APA, Harvard, Vancouver, ISO, and other styles
3

Nelson, M. T., and J. M. Quayle. "Physiological roles and properties of potassium channels in arterial smooth muscle." American Journal of Physiology-Cell Physiology 268, no. 4 (April 1, 1995): C799—C822. http://dx.doi.org/10.1152/ajpcell.1995.268.4.c799.

Full text
Abstract:
This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.
APA, Harvard, Vancouver, ISO, and other styles
4

Jimi, S., S. Takebayashi, S. Ryu, K. Saku, and N. Sakata. "Higher Migratory Activity of Arterial Smooth Muscle Cells Than of Venous Smooth Muscle Cells on Different Collagen Matrices." Phlebology: The Journal of Venous Disease 13, no. 3 (September 1998): 120–25. http://dx.doi.org/10.1177/026835559801300307.

Full text
Abstract:
Objective: To examine the biological differences between arteries and veins, we compared the migratory activities of arterial and venous smooth muscle cells (SMCs) using a modified Boyden chamber method. Design: Migratory activities of porcine arterial and venous smooth muscle cells (SMCs) were compared by a modified Boyden chamber method using coated filters with type I, III, IV and V collagens. Results: At the basal level of migration activity without stimulation, arterial SMCs showed greater migratory activity than venous SMCs in all of the substrata. When platelet-derived growth factor was added to the lower wells, all of the migration activities increased, and arterial SMCs showed significantly higher activity than venous SMCs. When cell-associated fibronectin was determined by an enzyme-linked immunoassay and immunohistochemistry, arterial SMCs secreted significantly more cell-associated fibronectin than venous SMCs. Type IV collagen had the greatest positive effect, and also induced the lowest level of cell-associated fibronectin. Conclusion: These in-vitro results indicate that fibronectin secreted by vascular smooth muscle is an important regulatory protein for cell migration even when SMCs migrate on collagen substrates. Arterial SMCs have higher migratory activities than venous SMCs as a result of their lower production of fibronectin.
APA, Harvard, Vancouver, ISO, and other styles
5

Wu, Kang, Haiyang Tang, Ruizhu Lin, Shane G. Carr, Ziyi Wang, Aleksandra Babicheva, Ramon J. Ayon, et al. "Endothelial platelet-derived growth factor-mediated activation of smooth muscle platelet-derived growth factor receptors in pulmonary arterial hypertension." Pulmonary Circulation 10, no. 3 (July 2020): 204589402094847. http://dx.doi.org/10.1177/2045894020948470.

Full text
Abstract:
Platelet-derived growth factor is one of the major growth factors found in human and mammalian serum and tissues. Abnormal activation of platelet-derived growth factor signaling pathway through platelet-derived growth factor receptors may contribute to the development and progression of pulmonary vascular remodeling and obliterative vascular lesions in patients with pulmonary arterial hypertension. In this study, we examined the expression of platelet-derived growth factor receptor isoforms in pulmonary arterial smooth muscle and pulmonary arterial endothelial cells and investigated whether platelet-derived growth factor secreted from pulmonary arterial smooth muscle cell or pulmonary arterial endothelial cell promotes pulmonary arterial smooth muscle cell proliferation. Our results showed that the protein expression of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell was upregulated in patients with idiopathic pulmonary arterial hypertension compared to normal subjects. Platelet-derived growth factor activated platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell, as determined by phosphorylation of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β. The platelet-derived growth factor-mediated activation of platelet-derived growth factor receptor α/platelet-derived growth factor receptor β was enhanced in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal cells. Expression level of platelet-derived growth factor-AA and platelet-derived growth factor-BB was greater in the conditioned media collected from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell than from normal pulmonary arterial endothelial cell. Furthermore, incubation of idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell with conditioned culture media from normal pulmonary arterial endothelial cell induced more platelet-derived growth factor receptor α activation than in normal pulmonary arterial smooth muscle cell. Accordingly, the conditioned media from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell resulted in more pulmonary arterial smooth muscle cell proliferation than the media from normal pulmonary arterial endothelial cell. These data indicate that (a) the expression and activity of platelet-derived growth factor receptor are increased in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal pulmonary arterial smooth muscle cell, and (b) pulmonary arterial endothelial cell from idiopathic pulmonary arterial hypertension patients secretes higher level of platelet-derived growth factor than pulmonary arterial endothelial cell from normal subjects. The enhanced secretion (and production) of platelet-derived growth factor from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell and upregulated platelet-derived growth factor receptor expression (and function) in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell may contribute to enhancing platelet-derived growth factor/platelet-derived growth factor receptor-associated pulmonary vascular remodeling in pulmonary arterial hypertension.
APA, Harvard, Vancouver, ISO, and other styles
6

Heller, Phillip F. "Paclitaxel and Arterial Smooth Muscle Cell Proliferation." Circulation 97, no. 16 (April 28, 1998): 1651. http://dx.doi.org/10.1161/01.cir.97.16.1651.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lee, Wen-Sen, Justin A. Harder, Masao YoshizuMi, Mu-En Lee, and Edgar Haber. "Progesterone inhibits arterial smooth muscle cell proliferation." Nature Medicine 3, no. 9 (September 1997): 1005–8. http://dx.doi.org/10.1038/nm0997-1005.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Reidy, Michael A., and David E. Bowyer. "Control of arterial smooth muscle cell proliferation." Current Opinion in Lipidology 4, no. 5 (October 1993): 349–54. http://dx.doi.org/10.1097/00041433-199310000-00002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hu, Zhan, Wendao Liu, Xiumeng Hua, Xiao Chen, Yuan Chang, Yiqing Hu, Zhenyu Xu, and Jiangping Song. "Single-Cell Transcriptomic Atlas of Different Human Cardiac Arteries Identifies Cell Types Associated With Vascular Physiology." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 4 (April 2021): 1408–27. http://dx.doi.org/10.1161/atvbaha.120.315373.

Full text
Abstract:
Objective: Although cellular heterogeneity within arterial walls has been explored in mice and nonhuman primates, the cellular composition of human arterial walls remains unclear. Approach and Results: The cellular composition of nondiseased cardiac arteries (3 aortas, 2 pulmonary arteries and 9 coronary arteries) from 3 heart transplantation patients were investigated by single-cell sequencing of >10 5 cells. Clustering analysis identified 25 subpopulations representing the 10 main arterial cell types: vascular smooth muscle cell (4 clusters), fibroblast (4 clusters), macrophage (Mφ, 4 clusters), T cell (4 clusters), endothelial cell (4 clusters), NK cell (2 clusters), mast cell (1 cluster), myofibroblast (1 cluster), oligodendrocyte (1 cluster), and B/plasma cells (1 cluster). Vascular smooth muscle cell was the largest cell population in cardiac arteries, followed by fibroblast, Mφ, T cell, endothelial cell, NK cell, and so on. We compared cellular composition among different arteries and found some artery-specific vascular smooth muscle cell and fibroblast subpopulations. The communication between vascular smooth muscle cell and fibroblast was predominant in nondiseased condition. Atherosclerosis-associated genes were particularly enriched in endothelial cell and Mφ, and intercellular communication between endothelial cell and immune cells was predicted to increase in atherosclerosis. The interaction between ICAM1 / VCAM1 (EC1) and ITGB2 (immune cells, especially inflammatory Mφ) was speculated to be essential for the pathogenesis of atherosclerosis. Conclusions: We created a cell atlas of human nondiseased cardiac arteries, and characterized the cellular compositions in different cardiac arteries. Our results could be used as a reference to identify vascular disease-associated cell populations and help investigate new therapeutic strategies for vascular diseases.
APA, Harvard, Vancouver, ISO, and other styles
10

Ashraf, Jasni Viralippurath, and Ayman Al Haj Zen. "Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10585. http://dx.doi.org/10.3390/ijms221910585.

Full text
Abstract:
Arteriogenesis is one of the primary physiological means by which the circulatory collateral system restores blood flow after significant arterial occlusion in peripheral arterial disease patients. Vascular smooth muscle cells (VSMCs) are the predominant cell type in collateral arteries and respond to altered blood flow and inflammatory conditions after an arterial occlusion by switching their phenotype between quiescent contractile and proliferative synthetic states. Maintaining the contractile state of VSMC is required for collateral vascular function to regulate blood vessel tone and blood flow during arteriogenesis, whereas synthetic SMCs are crucial in the growth and remodeling of the collateral media layer to establish more stable conduit arteries. Timely VSMC phenotype switching requires a set of coordinated actions of molecular and cellular mediators to result in an expansive remodeling of collaterals that restores the blood flow effectively into downstream ischemic tissues. This review overviews the role of VSMC phenotypic switching in the physiological arteriogenesis process and how the VSMC phenotype is affected by the primary triggers of arteriogenesis such as blood flow hemodynamic forces and inflammation. Better understanding the role of VSMC phenotype switching during arteriogenesis can identify novel therapeutic strategies to enhance revascularization in peripheral arterial disease.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Arterial Smooth Muscle Cell"

1

Arshad, Haroon. "Mathematical modelling of pulmonary arterial smooth muscle cell subtypes." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/mathematical-modelling-of-pulmonaryarterial-smooth-muscle-cell-subtypes(c1110807-d94d-487c-90b8-8714d5e42d16).html.

Full text
Abstract:
Alteration in the tone of pulmonary arteries may lead to disease such as pulmonary hypertension often associated with major cardiac complications. This dysfunction is partly in the pulmonary arterial smooth muscle cells (PASMCs) where the excitation-contraction coupling is modified by ion channel behaviour to increase the contractile force. Mathematical models of systemic smooth muscle cells (SMCs) that incorporate electrophysiological and chemomechanical mechanisms to understand the underlying cellular physiology have been successfully employed. Models of pulmonary arterial smooth muscle cells (PASMCs) are only beginning to emerge. Mathematical model prototyping with available experimental data and model investigation from different parameter values is a time-consuming and complex process. This thesis is concerned with the development and validation of mathematical models of excitation-contraction coupling in three types of PASMCs of the rat species, one homogeneous type originating from the distal pulmonary arteries and two from proximal pulmonary arteries. Some key novel additions from previous vascular SMC models include the distinct modelling of Ca2+ in the subplasmalemmal cytosolic region, incorporation of subunit-specific currents from the K+ channel family and a generic G-protein receptor model able to reproduce complex Ca2+ profiles. The main pulmonary and systemic arteries statistically differ in its response to phenylephrine in a wire myograph. The ionic currents of the models were validated against experimental data largely from rat species. The models replicate the recordings of Ca2+ and the resting potential (Em) profiles arising from agonist-induced cytosolic Ca2+ ([Ca2+]i) stimulation (G-protein activation), nifedipine, ryanodine, caffeine and niflumic acid. The distal PASMC model was sensitive to an increase in [Ca2+]i from G-protein activation although were less likely to reproduce Ca2+ oscillations than proximal PASMCs. The proximal models determined the likely proximal PASMC type in literature experiments recording [Ca2+]i and Em. I have developed software that enables other users to simulate Ca2+ and Em changes in SMC studies and the ability to parse a master file describing the mathematical model into different language formats to increase productivity. These models provide a foundation for further studies to better understand PASMC function in the context of normal physiology as well as pathological conditions.
APA, Harvard, Vancouver, ISO, and other styles
2

Beattie, David Keith. "The influence of altered haemodynamics on human smooth muscle cell behaviour." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369122.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hartley, S. A. "ATP regulated ion channels in arterial smooth muscle cells." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298264.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Curinga, Gabrielle Mercedes. "The role of runt-related transcription factor 2 in arterial smooth muscle cell mineralization /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/6353.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Izzard, Tanya. "Extracellular matrix and the cell cycle in vascular smooth muscle cells." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322616.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Suttie, Andrew William. "Allylamine toxicity and dedifferentiation of arterial smooth muscle cells in vitro." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390596.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Proudfoot, Diane. "Effects of macrophage factors on the growth of arterial smooth muscle cells." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321094.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wahl, Joel. "Development of Methods to Investigate Pulmonary Arterial Smooth Muscle Cells under Hypoxia." Licentiate thesis, Luleå tekniska universitet, Strömningslära och experimentell mekanik, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:ltu:diva-77140.

Full text
Abstract:
Hypoxic pulmonary vasoconstriction (HPV) is a physiological response to localized alveolarhypoxia that is intrinsic to the pulmonary circulation. By hypoxia-induced contractionof pulmonary arterial smooth muscle cells (PASMCs), the pulmonary capillary bloodflow is redirected to alveolar areas of high oxygen partial pressure, thus maintaining theventilation-perfusion ratio. Although the principle of HPV was recognized decades agothe underlying pathway remains elusive. The patch clamp technique, imaging and Ramanspectroscopy are methods that can be used to investigate parts of the mechanisms. Toenable measurements at controlled oxygen concentrations a gas-tight microfluidic systemwas developed. In this thesis preparatory experiments to couple the gas-tight systemto a microscope that enabled simultaneous measurements with patch clamp, imagingand Raman spectroscopy are discussed. The patch clamp technique is to be used formeasurements on the dynamics of the ion-channels in the cellular membrane as well aschanges in membrane potential as a response to hypoxia. Imaging of PASMCs is requiredto successfully apply the patch clamp technique. Further, imaging will also reveal whetherthe mechanical response of HPV has been triggered, for this purpose image analysis forestimation of optical flow can be used. Raman spectroscopy enables measurements ofbiochemical changes in redox biomarkers, cytochrome c and NADH, of the mitochondrialelectron transport chain. This thesis shows that the gas-tight microfluidic system providesoptimal control of the oxygen content, in an experimantal setting where the patch clamptechnique can be applied. Raman measurements showed significantly larger variationsin spectra compared to an open fluidic system, which is the conventional approach.However, the results showed a need for improved Raman preprocessing. For this purposea Convolutional Neural Network (CNN) was trained using synthetic spectra that providedoptimal reconstruction of the Raman signal. Finally, simultaneous imaging and Ramanspectroscopy of red blood cells were performed in a home built microscope. The resultspave the way for measurements on PASMCs.
APA, Harvard, Vancouver, ISO, and other styles
9

Winter, Polly. "Endothelial and smooth muscle cell-to-cell communication within rat small mesenteric arteries." Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436804.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Myllärniemi, Marjukka. "Regulation of arterial smooth muscle cell proliferation after endothelial injury : an experimental approach to restenosis and transplant arteriosclerosis." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/trans/vk/myllarniemi/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Arterial Smooth Muscle Cell"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

D, Huizinga Jan, ed. Pacemaker activity and intercellular communication. Boca Raton: CRC Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

Full text
Abstract:
Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Arterial Smooth Muscle Cell"

1

Bauriedel, Gerhard, Sven Schluckebier, Randolph Hutter, Ulrich Welsch, and Berndt Lüderitz. "Post-Angioplasty Smooth Muscle Cell Apoptosis." In Arterial Remodeling: A Critical Factor in Restenosis, 181–98. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6079-1_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Hüttner, I., O. Kocher, and G. Gabbiani. "Endothelial and Smooth-Muscle Cells." In Diseases of the Arterial Wall, 3–41. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1464-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Quayle, J. M., and M. T. Nelson. "Calcium Channels in Arterial Smooth Muscle Cells." In Ion Flux in Pulmonary Vascular Control, 41–47. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2397-0_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Wu, K. K. "Prostacyclin and nitric oxide-related gene transfer in preventing arterial thrombosis and restenosis." In Prostaglandins and Control of Vascular Smooth Muscle Cell Proliferation, 107–23. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-7352-9_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Tiozzo, R., M. R. Cingi, D. Reggiani, and S. Calandra. "Glycosaminoglycans and the proliferation of arterial smooth muscle cells." In Atherosclerosis and Cardiovascular Disease, 337–44. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0731-7_44.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Nilsson, Jan, and Anna Hultgårdh Nilsson. "Regulation of Arterial Smooth Muscle Cell Proliferation during Development and Lesion Formation." In Genetic factors in coronary heart disease, 337–49. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bhalla, Ramesh C., Lusiane M. Bendhack, and Ram V. Sharma. "Cell Membrane Properties of the Arterial Smooth Muscle from Spontaneously Hypertensive Rats." In Essential Hypertension 2, 175–90. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Nelson, Mark T., Nicholas B. Standen, Joseph E. Brayden, and Jennings F. Worley. "Membrane Potential and Calcium Channels in Arterial Smooth Muscle Cells." In Essential Hypertension 2, 37–44. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ludewig, Burkhard. "Tracking Arterial Smooth Muscle-Specific T Cells in the Inflamed Vasculature." In Advances in Experimental Medicine and Biology, 183–89. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0757-4_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Declerck, Ingrid, Guy Droogmans, and Rik Casteels. "Excitatory Agonists and Ca-Permeable Channels in Arterial Smooth Muscle Cells." In Essential Hypertension 2, 45–56. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Arterial Smooth Muscle Cell"

1

van den Broek, Chantal, Jeroen Nieuwenhuizen, Marcel Rutten, and Frans van de Vosse. "Mechanical Characterization of Vascular Smooth Muscle." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53434.

Full text
Abstract:
Remodeling of the arterial wall, in response to e.g. induced hypertension, vasoconstriction, and reduced cyclic stretch, has been studied in detail to get insight into vascular pathologies [1]. Constitutive models are helpful to the understanding of the relation between different processes that occur in the arterial wall during remodeling. Including the smooth muscle cell (SMC) behavior in constitutive models is relevant, as those cells may change tone when subjected to an altered mechanical loading and can initiate arterial remodeling.
APA, Harvard, Vancouver, ISO, and other styles
2

BLAES, N., and C. COVACHO. "PLATELET AGGREGATION INDUCED BY TUMORIGENIC ARTERIAL SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643413.

Full text
Abstract:
A focal proliferation of intimal smooth muscle cells is assumed to be an early event in atherogenesis. In addition, platelets have been suggested to play a role at different steps of the disease process. Blood platelets can be aggregated by a number of tumor cells of various tissue origin. Rat arterial smooth muscle cells presenting a tumorigenic and metastatic phenotype (NBC1 and NBC2 cell lines) have been obtained in the laboratory (BLAES N. et al, Arch. Mai. Coeur Vais., 1986, 79, 55a). The aim of the present work was to assay the proaggregant abilities of these tumor cells of vascular origin. Smooth muscle cells derived from normal rat aortic media. NBC1 and NBC2 cells were spontaneously transformed in cell culture. Interactions between cells and platelets were studied in an homologous in vitro system containing 0.5 ml of PRP (300 000 platelets per ul) from heparinized rat blood and 50 ul of rat smooth muscle cells suspension. Proaggregant activity was tested for control non tumorigenic smooth muscle cells and tumorigenic cells (after 10 or 240 passages). Experiments showed that NBC2 cells elicited a proaggregant ability, weak after 10 passages but very significant after 240 passages. This effect depended on the number of cells added to the platelet suspension (it increased from 105 to 2.106 cells per 0.5 ml suspension). Aggregation profiles appeared biphasic and could be abolished by aspirin. The first reversible phase occured immediately and was reduced dose-dependently by apyrase. Hirudin was shown to affect the aggregation profile suggesting an activation of the clotting system in the NBC2-induced platelet activation. By comparison, non tumorigenic arterial smooth muscle cells showed no effect at comparable cell numbers and NBC1 cells (less metastatic than NBC2 cells) exhibited only a monophasic profile. These results suggest that NBC2 cells are able to induce platelet aggregation by mechanisms involving ADP and thrombin generation. This ability could be related to their tumorigenic and metastatic phenotype.
APA, Harvard, Vancouver, ISO, and other styles
3

Scott, Devon, Robin Shandas, and Wei Tan. "Effect of Vessel Stiffening and High Pulsatility Flow on Contractile Function and Proliferation of Small Arterial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19597.

Full text
Abstract:
Recent studies have identified arterial stiffening as a predictor of some vascular diseases such as pulmonary hypertension, which is characterized by dysfunction of small arteries. Stiffening is shown to cause changes in blood flow, extending high pulsatile flow into small arteries that normally experience steady flow conditions (Chui 2004). However, few studies have investigated the mechanisms underlying the effects of arterial stiffening on vascular remodeling. We hypothesized that arterial stiffness effects dysfunction of downstream vascular endothelium and smooth muscle through changes in flow pulsatility. Previously we developed a flow system to study the influence of pulse flow waves, by modulating upstream stiffness, on downstream mimetic vascular cell co-culture. With this system, the present study examines contractile and proliferating protein expressions of smooth muscle cell (SMC) co-cultured with endothelial cell (EC). The endothelium, directly interfaces with the blood flow, and transduces mechanical signals to underlying SMC (Stegemann 2005). We recently showed that high pulsatile flow induced EC dysfunction. Therefore, we further asked whether high pulsatility flow would cause characteristic changes of small arterial SMC in the hypertension condition such as smooth muscle hyperplasia (increased cell proliferation) and hypertrophy (increased contractile proteins) (Voelkel 1997), and whether these changes would be mediated by EC dysfunction.
APA, Harvard, Vancouver, ISO, and other styles
4

Tamura, Yuichi, Ly Tu, Tsunehisa Yamamoto, Carole Phan, Raphael Thuillet, Alice Huertas, Morane Le Hiress, Elie Fadele, Marc Humbert, and Christophe Guignabert. "Uric acid causes excessive pulmonary arterial smooth muscle cell proliferationviaURATv1 upregulation in pulmonary arterial hypertension." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5102.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Asada, Y., T. Hayashi, and A. Sumiyoshi. "ENDOTHELIAL CELL INJURIES AND SMOOTH MUSCLE CELL PROLIFERATION INDUCED BY MATERIALS RELEASED FROM PLATELET-RICH THROMBUS IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644601.

Full text
Abstract:
It is widely held that the disturbance in the integrity of the arterial endothelium may lead to the development of arteriosclerosis and many factors have been postulated to cause the endothelial injury, such as hemodynamic stress, anoxia, platelet-releasing materials, and so on. However, whether any of these is important for endothelial injury is unclear. We studied whether the released products from activated platelets and/or thrombi could cause endothelial damage and proliferation of smooth muscle cells in large vessels in vivo.Polyethylene tubing was inserted into the ascending aorta of rabbits via the common carotid artery and placed for one, 4, and 24 weeks continuously to induce vessel wall injury and thrombotic events. Then the direct non-injured segments from the descending thoracic and abdominal aorta was morphologically examined, and 3H-thymidine incorporation into the arterial wall was also examined. The descending aortas of experimental rabbits showed endothelial damage and increased mitoses of endothelial cells. Modified smooth muscle cells were noted in the subendothelial layer, and 3H-thymidine incorporation into the intima and media significantly increased in the experimental group at one week(Fig.). At 24 weeks, the intimal thickening with smooth muscle cell proliferation was also found.This experiment indicates that materials released from the activated platelets and/or thrombi into the circulation can cause endothelial damage and smooth muscle cell proliferation and intimal thickening at downstream and remote aortic segments.
APA, Harvard, Vancouver, ISO, and other styles
6

Hosokawa, Susumu, Akihito Sasaki, Go Haraguchi, Mitsuaki Isobe, and Shozaburo Doi. "Novel Selective NFºB Inhibitor Compound Suppresses Pulmonary Arterial Smooth Muscle Cell Proliferation For Pulmonary Arterial Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3406.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

DeClerck, Y. A., R. Bock, and W. E. Laug. "PRODUCTION OF A TISSUE INHIBITOR OF METALLOPROTEINASES BY BOVINE VASCULAR CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644603.

Full text
Abstract:
Tissue Inhibitor of Metalloproteinases (TIMP) plays an important role in collagen turnover in tissue due to its ability to irreversibly inhibit mammalian collagenases. We have investigated the production of such an inhibitor by various cells of bovine vessels including endothelial cells of arterial, venous and capillary origin and arterial smooth muscle cells. While large amounts of collagenase inhibitor (800 mU/106 cells/24 hr) were produced by vascular smooth muscle cells, smaller amounts were detected in* the medium conditioned by either arterial, capillary or venous endothelial cells (90, 1.7 and 1.1 mU/106 cells/24 hr respectively). An inhibitor with a Mr of 28,500 was purified from serum free medium conditioned by bovine smooth muscle cells using molecular sieve followed by heparin sepharose and carboxy-methylcellulose chromatography. It inhibited several vertebrate collagenases but was inactive against bacterial collagenase. This inhibitor was resistant to treatment with acid and heat but sensitive to trypsin and reduction alkylation. It formed with vertebrate collagenase an enzyme-inhibitor complex resistant to organomercurials or trypsin. This inhibitor, therefore, is similar to a collagenase inhibitor produced by human fibroblasts and a tissue inhibitor of metalloproteinases extracted from human amniotic fluid and rabbit bone.The production of TIMP by bovine vascular smooth muscle cells markedly increased during cell proliferation. In addition, when endothelial cells were grown on a preformed layer of smooth muscle cells, the production of TIMP was more than additive suggesting an enhancing effect of endothelial cells on vascular smooth muscle cells.These data suggest that the large amount of TIMP produced by vascular muscle cells may be responsible for the accumulation of collagen characteristically observed in conjunction with smooth muscle cells hyperplasia in atherosclerotic plaques.
APA, Harvard, Vancouver, ISO, and other styles
8

Espinosa, Gabriela, Lisa Bennett, William Gardner, and Jessica Wagenseil. "The Effects of Extracellular Matrix Protein Insufficiency and Treatment on the Stiffness of Arterial Smooth Muscle Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14131.

Full text
Abstract:
Increased arterial stiffness is directly correlated with hypertension and cardiovascular disease. Stiffness of the conducting arteries is largely determined by the extracellular matrix (ECM) proteins in the wall, such as collagen and elastin, produced by the smooth muscle cells (SMCs) found in the medial layer. Elastin is deposited as soluble tropoelastin and is later crosslinked into elastin fibers. Newborn mice lacking the elastin protein ( Eln−/−) have increased arterial wall stiffness and SMCs with altered proliferation, migration and morphology [1]. Vessel elasticity is also mediated by other ECM proteins, such as fibulin-4. Elastic tissue, such as lung, skin, and arteries, from fibulin-4 deficient ( Fbln4−/−) mice show no decrease in elastin content, but have reduced elasticity due to disrupted elastin fibers [2]. Arteries from both elastin and fibulin-4 deficient mice have been previously studied, but the mechanical properties of their SMCs have not been investigated. Recent experiments comparing arterial SMCs from old and young animals suggest that mechanical properties of the SMCs themselves may contribute to changes in wall stiffness [3]. Hence, we investigated the stiffness of isolated arterial SMCs from elastin and fibulin-4 deficient mice using atomic force microscopy (AFM). In addition, we studied the effects of two elastin treatments on the mechanical properties of SMCs from Eln+/+ and Eln−/− mice. Differences between the treatments may elucidate the importance of soluble versus crosslinked elastin on single cell stiffness.
APA, Harvard, Vancouver, ISO, and other styles
9

Han, Hai-Chao, Raymond P. Vito, Kristin Michael, and David N. Ku. "Axial Stretch Increases Cell Proliferation in Arteries in Organ Culture." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2516.

Full text
Abstract:
Abstract To study the effect of axial stretch on vascular function and wall remodeling, porcine carotid arteries were cultured under conditions of physiological flow and elevated axial stretch in an ex vivo organ culture system. Smooth muscle cell proliferation was measured by bromodeoxyuridine index. Results showed that cell proliferation was significantly increased in the highly stretched arteries when compared to the normally stretched arteries. This may indicate the feasibility of stimulating new arterial growth by stretching natural arteries.
APA, Harvard, Vancouver, ISO, and other styles
10

Venkatasubramanian, Ramji, Wim Wolkers, Charles Soule, Paul Iaizzo, and John Bischof. "Effect of Tissue Dehydration on Smooth Muscle Cell Contractility, Collagen Matrix Structure and Overall Artery Biomechanics." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192346.

Full text
Abstract:
Applications involving freeze-thaw in arteries such as cryoplasty and cryopreservation alter the arterial biomechanics significantly [1]. Tissue dehydration or bulk water loss is observed following freeze-thaw in native arteries as well as other artificial tissues [1, 2]. It is hypothesized that tissue dehydration observed during freeze-thaw is an important mechanism underlying the biomechanical changes in arteries. In order to test this hypothesis, dehydration was induced in arteries (without changing temperature or phase) by treating them with different concentrations of hyperosmotic mannitol solutions. Changes to smooth muscle cell (SMC) contractility, collagen matrix structure and overall artery biomechanics were studied following tissue dehydration. SMC contractility and relaxation were measured by studying the response of arteries to norepinephrine (NE) and acetylcholine (AC) respectively. Collagen matrix structure was assessed by studying the thermal denaturation of collagen due to heating using Fourier transform infrared (FTIR) spectroscopy and the overall artery biomechanics through uniaxial tensile tests.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Arterial Smooth Muscle Cell' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography