Relevant bibliographies by topics / Vascular smooth muscle cell

Academic literature on the topic 'Vascular smooth muscle cell'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Vascular smooth muscle cell"

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Fiedler, Jan, and Thomas Thum. "Vascular Smooth Muscle Cell Remodeling." Circulation Research 123, no. 12 (December 7, 2018): 1261–63. http://dx.doi.org/10.1161/circresaha.118.314184.

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Clark, T., P. K. Ngai, C. Sutherland, U. Gröschel-Stewart, and M. P. Walsh. "Vascular smooth muscle caldesmon." Journal of Biological Chemistry 261, no. 17 (June 1986): 8028–35. http://dx.doi.org/10.1016/s0021-9258(19)57507-x.

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Miano, Joseph M. "Vascular smooth muscle cell differentiation – 2010." Journal of Biomedical Research 24, no. 3 (May 2010): 169–80. http://dx.doi.org/10.1016/s1674-8301(10)60026-7.

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Chistiakov, D. A., A. N. Orekhov, and Y. V. Bobryshev. "Vascular smooth muscle cell in atherosclerosis." Acta Physiologica 214, no. 1 (February 25, 2015): 33–50. http://dx.doi.org/10.1111/apha.12466.

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Harman, J. L., E. Loche, A. Dalby, and H. F. Jørgensen. "Vascular smooth muscle cell gene regulation." Atherosclerosis 237, no. 2 (December 2014): e10. http://dx.doi.org/10.1016/j.atherosclerosis.2014.10.060.

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Wang, Cecilia C. Low, Victor Sorribas, Girish Sharma, Moshe Levi, and Boris Draznin. "Insulin attenuates vascular smooth muscle calcification but increases vascular smooth muscle cell phosphate transport." Atherosclerosis 195, no. 1 (November 2007): e65-e75. http://dx.doi.org/10.1016/j.atherosclerosis.2007.02.032.

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Yao, C. C., J. Breuss, R. Pytela, and R. H. Kramer. "Functional expression of the alpha 7 integrin receptor in differentiated smooth muscle cells." Journal of Cell Science 110, no. 13 (July 1, 1997): 1477–87. http://dx.doi.org/10.1242/jcs.110.13.1477.

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Expression of the alpha7 integrin is developmentally regulated and is thought to be tissue-specific for both skeletal and cardiac muscles. We now report that alpha7 is also strongly and ubiquitously expressed by various types of smooth muscle, including vascular, gastrointestinal and genitourinary smooth muscles. In addition, alpha7 was surface-expressed by a number of smooth muscle cell lines that maintained their differentiated phenotype following adaptation to culture. Studies with the mouse 9E11G smooth muscle cell line showed that the alpha7 integrin mediated both adhesion and motility of these cells on laminin 1 substrates. Alpha7 expression appears to correlate with the smooth-muscle-differentiated phenotype. The multipotential P19 mouse embryonic stem cell line lacks alpha7 but uses the alpha6 integrin to adhere to laminin 1. Following retinoic acid-induced P19 differentiation predominantly to the smooth muscle cell lineage, high expression of alpha7 was detected along with partial dependence on alpha7 for binding to laminin. The expression of alpha7 paralleled the induction of smooth-muscle-specific alpha-actin, as revealed by dual-labeling flow cytometry. In contrast, alpha7, which initially was highly expressed on the surface of vascular smooth muscle cell explants, was rapidly downregulated in smooth muscle cell outgrowths as they dedifferentiated into their synthetic phenotype. The results indicate that the expression of alpha7 integrin in smooth muscle cells is associated with their differentiated phenotype and mediates their interaction with laminins.
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Leopold, Jane A. "Vascular calcification: Mechanisms of vascular smooth muscle cell calcification." Trends in Cardiovascular Medicine 25, no. 4 (May 2015): 267–74. http://dx.doi.org/10.1016/j.tcm.2014.10.021.

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Gochuico, Bernadette R., Jie Zhang, Bei Yang Ma, Ann Marshak-Rothstein, and Alan Fine. "TRAIL expression in vascular smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 5 (May 1, 2000): L1045—L1050. http://dx.doi.org/10.1152/ajplung.2000.278.5.l1045.

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TRAIL is a cell-associated tumor necrosis factor-related apoptosis-inducing ligand originally identified in immune cells. The ligand has the capacity to induce apoptosis after binding to cell surface receptors. To examine TRAIL expression in murine vascular tissue, we employed in situ hybridization and immunohistochemistry. In these studies, we found that TRAIL mRNA and protein were specifically localized throughout the medial smooth muscle cell layer of the pulmonary artery. Notably, a similar pattern of expression was observed in the mouse aorta. Consistent with these findings, we found that cultures of primary human aorta and pulmonary artery smooth muscle cells express abundant TRAIL mRNA and protein. We also found that these cells and endothelial cells undergo cell lysis in response to exogenous addition of TRAIL. Last, we confirmed that TRAIL specifically activated a death program by confirming poly(ADP ribose) polymerase cleavage. Overall, we believe that these findings are relevant to understanding the factors that regulate cell turnover in the vessel wall.
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Vouyouka, Angela G., Yan Jiang, and Marc D. Basson. "Pressure alters endothelial effects upon vascular smooth muscle cells by decreasing smooth muscle cell proliferation and increasing smooth muscle cell apoptosis." Surgery 136, no. 2 (August 2004): 282–90. http://dx.doi.org/10.1016/j.surg.2004.04.033.

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Dissertations / Theses on the topic "Vascular smooth muscle cell"

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Fellows, Adam Lee. "FOXO3a in vascular smooth muscle cell apoptosis." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275687.

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FOXO3a is a pro-apoptotic transcription factor which shows increased activation in vascular smooth muscle cells (VSMCs) of advanced atherosclerotic plaques, specifically within the intimal layer. Since VSMC apoptosis plays a crucial role in the pathophysiology of atherosclerosis, we investigated the mechanisms underlying FOXO3a-mediated cell death in this particular cell type. We aimed to characterise a novel VSMC system (FOXO3aA3ERTM) and use these cells to validate MMP-13 and TIMP3 as new FOXO3a target genes. Also, we sought to determine the mechanisms of FOXO3aA3ERTM-mediated VSMC apoptosis, particularly regarding MMP-13 and TIMP3, potential MMP-13 substrates in the extracellular matrix and the precise apoptotic signalling involved. Furthermore, we aimed to investigate whether VSMC-specific activation of FOXO3aA3ERTM in mouse affects vascular remodelling during injury and whether this is reliant on MMP-13. Lastly, we aimed to address if endogenous FOXO3a upregulates MMP-13 in mouse and human VSMCs. Our laboratory has created a transgenic rat VSMC line which stably expresses an inducible FOXO3a mutant allele known as FOXO3aA3ERTM and previous microarray experiments identified matrix metalloproteinase 13 (MMP-13) as a potential novel FOXO3a target gene. Initially, we described several key features of the FOXO3aA3ERTM VSMCs used throughout this thesis, and subsequently demonstrated that MMP-13 is a bona fide target whose expression is rapidly upregulated upon FOXO3a activation, leading to markedly higher levels of protein, cleavage and proteolytic capacity. This induction of MMP-13 was responsible for the vast majority of FOXO3a-mediated apoptosis which was accompanied by prominent degradation of fibronectin, a glycoprotein found in the extracellular matrix. However, we could not identify a terminal apoptotic pathway. FOXO3a also downregulated the endogenous MMP inhibitor TIMP3, the recombinant protein of which reduced both MMP-13 proteolysis and FOXO3a-mediated apoptosis. Activation of FOXO3aA3ERTM in the VSMCs of medium and large arteries in mice resulted in heightened expression of MMP-13 in the vessel wall, which contributed to enhanced neointimal formation during carotid ligation. Finally, endogenous FOXO3a activation leads to increased MMP-13 expression in human VSMCs, but not mouse. Overall, we have shown that FOXO3a promotes VSMC apoptosis through MMP-13 both in vitro and in vivo, a novel pathway that has important implications for the pathogenesis and treatment of vascular disease.
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Zhao, Ning. "Notch Signaling Guides Vascular Smooth Muscle Cell Function." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396890017.

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Wong, Wai-ming. "Effects of isoflavonoids on vascular smooth muscle cell proliferation /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433913.

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Lugano, Roberta. "Low density lipoproteins, vascular smooth muscle cell function and vascular remodeling." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283471.

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High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors. Hypercholesterolemia induces endothelial dysfunction and chronic intimal inflammatory cell accumulation, hallmarks of the initiation of atherosclerosis. Additionally, growing human atherosclerotic plaques show proliferation and migration of vascular smooth muscle cells (VSMC) towards the intima producing remodeling of the vascular wall. However, those plaques that are most prone to rupture show a progressive loss of VSMC becoming soft and vulnerable and these lipid-rich high risk plaques cause clinical episodes resulting in morbid or fatal ischemic events. The mechanisms involved in the transformation of a plaque into a vulnerable VSMC-depleted atheroma have not been completely elucidated. Lipid-rich-VSMC have an impaired vascular repair function due to changes in cytoskeleton proteins. However, the effects of LDL on VSMC function during plaque remodeling and vascular repair are not fully understood. Thus, the aim of this thesis was to investigate early changes directly induced by LDL on VSMC phenotype and function and to identify the molecular mechanisms involved. This thesis demonstrates that the cardiovascular risk of hypercholesterolemia involves the interaction of LDL with VSMC and the regulation at a molecular level of different pathways that converge in the cell’s migratory capacity. Migratory function of lipid-loaded VSMC can be restored by inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) through a Rho kinase and myosin light chain phosphatase dependent mechanism. In addition, the studies performed in this thesis show that LDL affect VSMC adhesion, migration and cytoskeleton dynamics through the abrogation of the urokinase-plasminogen activator (uPA)/uPA receptor (uPAR) system function and by modulation of HSP27 phosphorylation and subcellular localization.
El nivel elevado de lipoproteínas de baja densidad (LDL), uno de los principales factores de riesgo cardiovascular, conllevan a una disfunción endotelial y acumulación crónica de células inflamatorias en la íntima arterial en la etapa inicial de desarrollo de la arterosclerosis. Además, la progresión de las placas arterioscleróticas se caracteriza por un proceso de remodelado vascular consecuencia de la proliferación y migración de células musculares lisas vasculares (CML) en la íntima. Sin embargo, las placas ateroscleróticas con mayor susceptibilidad a la ruptura presentan una pérdida progresiva de CML, siendo estas placas ricas en lípidos y altamente vulnerables las que provocan eventos isquémicos mórbidos o fatales. Hoy día desconocemos todavía los mecanismos involucrados en la transformación de las placas en ateromas vulnerables. Las CML ricas en lípidos presentan alteraciones en su capacidad de reparación vascular debido a alteraciones en proteínas del citoesqueleto. Sin embargo, los efectos de las LDL en la función de las CML durante el remodelado de las placas y reparación vascular se desconocen en gran medida. Por ello, el objetivo de esta tesis ha sido investigar los cambios iniciales inducidos directamente por las LDL en el fenotipo y la función de las CML e identificar los mecanismos moleculares involucrados. Esta tesis demuestra que el riesgo cardiovascular de la hipercolesterolemia implica la interacción entre LDL y CML y la regulación a nivel molecular de diferentes vías de señalización que convergen en la migración celular. La capacidad de migración de CML cargadas de lípidos puede restituirse mediante la inhibición de la 3-hidroxi-3-metilglutaril coenzima-A (HMG-CoA), a través de un mecanismo dependiente de la quinasa Rho. Además, los estudios realizados en esta tesis demuestran que las LDL afectan la adhesión, migración y dinámica de formación del citoesqueleto de las CML a través de la alteración de la función del sistema del activador del plasminogeno tipo uroquinasa (uPA)/uPA receptor (uPAR) y mediante la modulación de la fosforilación y localización subcelular de la HSP27.
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Lugano, Roberta 1983. "Low density lipoproteins, vascular smooth muscle cell function and vascular remodeling." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283471.

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High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors. Hypercholesterolemia induces endothelial dysfunction and chronic intimal inflammatory cell accumulation, hallmarks of the initiation of atherosclerosis. Additionally, growing human atherosclerotic plaques show proliferation and migration of vascular smooth muscle cells (VSMC) towards the intima producing remodeling of the vascular wall. However, those plaques that are most prone to rupture show a progressive loss of VSMC becoming soft and vulnerable and these lipid-rich high risk plaques cause clinical episodes resulting in morbid or fatal ischemic events. The mechanisms involved in the transformation of a plaque into a vulnerable VSMC-depleted atheroma have not been completely elucidated. Lipid-rich-VSMC have an impaired vascular repair function due to changes in cytoskeleton proteins. However, the effects of LDL on VSMC function during plaque remodeling and vascular repair are not fully understood. Thus, the aim of this thesis was to investigate early changes directly induced by LDL on VSMC phenotype and function and to identify the molecular mechanisms involved. This thesis demonstrates that the cardiovascular risk of hypercholesterolemia involves the interaction of LDL with VSMC and the regulation at a molecular level of different pathways that converge in the cell’s migratory capacity. Migratory function of lipid-loaded VSMC can be restored by inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) through a Rho kinase and myosin light chain phosphatase dependent mechanism. In addition, the studies performed in this thesis show that LDL affect VSMC adhesion, migration and cytoskeleton dynamics through the abrogation of the urokinase-plasminogen activator (uPA)/uPA receptor (uPAR) system function and by modulation of HSP27 phosphorylation and subcellular localization.
El nivel elevado de lipoproteínas de baja densidad (LDL), uno de los principales factores de riesgo cardiovascular, conllevan a una disfunción endotelial y acumulación crónica de células inflamatorias en la íntima arterial en la etapa inicial de desarrollo de la arterosclerosis. Además, la progresión de las placas arterioscleróticas se caracteriza por un proceso de remodelado vascular consecuencia de la proliferación y migración de células musculares lisas vasculares (CML) en la íntima. Sin embargo, las placas ateroscleróticas con mayor susceptibilidad a la ruptura presentan una pérdida progresiva de CML, siendo estas placas ricas en lípidos y altamente vulnerables las que provocan eventos isquémicos mórbidos o fatales. Hoy día desconocemos todavía los mecanismos involucrados en la transformación de las placas en ateromas vulnerables. Las CML ricas en lípidos presentan alteraciones en su capacidad de reparación vascular debido a alteraciones en proteínas del citoesqueleto. Sin embargo, los efectos de las LDL en la función de las CML durante el remodelado de las placas y reparación vascular se desconocen en gran medida. Por ello, el objetivo de esta tesis ha sido investigar los cambios iniciales inducidos directamente por las LDL en el fenotipo y la función de las CML e identificar los mecanismos moleculares involucrados. Esta tesis demuestra que el riesgo cardiovascular de la hipercolesterolemia implica la interacción entre LDL y CML y la regulación a nivel molecular de diferentes vías de señalización que convergen en la migración celular. La capacidad de migración de CML cargadas de lípidos puede restituirse mediante la inhibición de la 3-hidroxi-3-metilglutaril coenzima-A (HMG-CoA), a través de un mecanismo dependiente de la quinasa Rho. Además, los estudios realizados en esta tesis demuestran que las LDL afectan la adhesión, migración y dinámica de formación del citoesqueleto de las CML a través de la alteración de la función del sistema del activador del plasminogeno tipo uroquinasa (uPA)/uPA receptor (uPAR) y mediante la modulación de la fosforilación y localización subcelular de la HSP27.
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Wong, Wai-ming, and 黃慧明. "Effects of isoflavonoids on vascular smooth muscle cell proliferation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45011059.

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Havrda, Matthew C. "Molecular Mechanisms of Notch Signaling Governing Vascular Smooth Muscle Cell Proliferation." Fogler Library, University of Maine, 2006. http://www.library.umaine.edu/theses/pdf/HavrdaMC2006.pdf.

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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.

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Haider, Ursula G. B. "Resveratrol Attenuates Vascular Smooth Muscle Cell Hypertrophy and Hyperplasia." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-8688.

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Kemp, Christian R. W. "Mechanical influences on human vascular smooth muscle cell growth." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29397.

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The leading cause of death in Western countries is cardiovascular disease with over 1 million people dying each year as a result in the United States alone. One condition identified as a risk factor for cardiovascular disease is an increased blood pressure or "hypertension" which has been shown to result in morphological changes in blood vessels at different sites around the body, including narrowing of pre-capillary "resistance" vessels. This thesis has sought to investigate whether or not this narrowing of resistance vessels might result from the increased physical forces of hypertension exerted upon the vascular smooth muscle cells of the vessel wall and to investigate the intracellular signalling mechanisms initiating this cellular response. Results indicate that cultured human vascular smooth muscle cells undergo cellular proliferation in response to chronic cyclical mechanical strain but only in the presence of suitable concentrations of soluble growth factors. Furthermore, these growth factors do not originate from the cells in response to the mechanical strain. Therefore, the proliferation is a direct response proportional to the strain applied but dependent upon the concentration of growth factors in the overlying media. In addition the magnitude of human vascular smooth muscle cell proliferation in response to mechanical strain is dependent upon interactions between the cells and specific extracellular matrix proteins and involves activation of the mitogen-activating protein kinase intracellular signalling cascade. In conclusion, these results suggest that the narrowing of resistance vessels observed in hypertension subjects may be a direct result of the increased physical forces exerted upon the vascular smooth muscle cells in conjunction with circulating growth factors. This biological response is mediated via specific cell/matrix interactions and involves specific intracellular signalling pathways, which may provide new targets for the effective treatment and/or management of these structural alterations observed in hypertension individuals.
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Books on the topic "Vascular smooth muscle cell"

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

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

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

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Book chapters on the topic "Vascular smooth muscle cell"

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Campbell, Gordon R., Johnny L. Efendy, and Julie H. Campbell. "Vascular Smooth Muscle Cells." In Pan Vascular Medicine, 205–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56225-9_12.

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Riascos-Bernal, Dario F., and Nicholas E. S. Sibinga. "Vascular Smooth Muscle Cells." In Atherosclerosis, 117–28. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch10.

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Proudfoot, Diane, and Catherine Shanahan. "Human Vascular Smooth Muscle Cell Culture." In Methods in Molecular Biology, 251–63. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-367-7_17.

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Takagi, Yasushi. "Vascular Smooth Muscle Cell-Related Molecules and Cells." In Moyamoya Disease Update, 69–72. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99703-0_11.

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Highsmith, Robert F., and Oliver M. FitzGerald. "Endothelial Cell Regulation of Vascular Smooth Muscle." In Physiology and Pathophysiology of the Heart, 755–71. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_37.

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Leopold, Jane A., and Joseph Loscalzo. "Vascular Smooth Muscle Cell Biology and Restenosis." In Applications of Antisense Therapies to Restenosis, 45–69. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5183-6_4.

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Owens, Gary K. "Molecular Control of Vascular Smooth Muscle Cell Differentiation and Phenotypic Plasticity." In Vascular Development, 174–93. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470319413.ch14.

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Kent, T. A., A. Jazayeri, and J. M. Simard. "Serotonin as a Vascular Smooth Muscle Cell Mitogen." In Serotonin: Molecular Biology, Receptors and Functional Effects, 398–405. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7259-1_39.

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Dash, Biraja C. "Induced Pluripotent Stem Cell-Derived Vascular Smooth Muscle Cells for Vascular Regeneration." In Stem Cell Therapy for Vascular Diseases, 199–219. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56954-9_9.

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Engel, Leslie, Eric Choi, Kay Broschat, Chris Gorka, Una Ryan, and Allan Callow. "The Role of the α vB3 Integrin in Smooth Muscle Cell Migration." In Vascular Endothelium, 167–68. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3_26.

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Conference papers on the topic "Vascular smooth muscle cell"

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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.

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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.
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Tsvankin, Vadim, Dmitry Belchenko, Devon Scott, and Wei Tan. "Anisotropic Strain Effects on Vascular Smooth Muscle Cell Physiology." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176284.

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Biological development is a complex and highly-regulated process, a significant part of which is controlled by mechanostimulus, or the strain imparted on a cell by its environment. Mechanostimulus is important for stem cell differentiation, from cytoskeletal assembly to cell-cell and cell-matrix adhesion [1]. The mechanics of cells and tissues play a critical role in organisms, under both physiological and pathological conditions; abnormal mechanotransduction — the mechanism by which cells sense and respond to strain — has been implicated in a wide range of clinical pathologies [2,3].
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Kohn, Julie C., Francois Bordeleau, and Cynthia A. Reinhart-King. "Vascular Smooth Muscle Cell Matrix-Degradation by Podosomes." In 2013 39th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2013. http://dx.doi.org/10.1109/nebec.2013.151.

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Ahsan, Taby, Adele M. Doyle, Garry P. Duffy, Frank Barry, and Robert M. Nerem. "Stem Cells and Vascular Regenerative Medicine." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193591.

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Vascular applications in regenerative medicine include blood vessel substitutes and vasculogenesis in ischemic or engineered tissues. For these repair processes to be successful, there is a need for a stable supply of endothelial and smooth muscle cells. For blood vessel substitutes, the immediate goal is to enable blood flow, but vasoactivity is necessary for long term success. In engineered vessels, it is thought that endothelial cells will serve as an anti-thrombogenic lumenal layer, while smooth muscle cells contribute to vessel contractility. In other clinical applications, what is needed is not a vessel substitute but the promotion of new vessel formation (vasculogenesis). A simplified account of vasculogenesis is that endothelial cells assemble to form vessel-like structures that can then be stabilized by smooth muscle cells. Overall, the need for new vasculature to transfer oxygen and nutrients is important to reperfuse not only ischemic tissue in vivo, but also dense, structurally complex engineered tissue. The impact of these vascular therapies, however, is limited in part by the low yield and inadequate in vitro proliferation potential of primary endothelial and smooth muscle cells. Thus, there is a need to address the cell sourcing issue for vascular cell-based therapies, potentially using stem cells.
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Sariipek, N., S. Seeherman, V. Rybka, N. Shults, S. Gychka, and Y. Suzuki. "Tau Protein in Vascular Smooth Muscle Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2107.

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Grasso, Michael A., Yelena Yesha, Ronil Mokashi, Darshana Dalvi, Antonio Cardone, Alden A. Dima, Kiran Bhadriraju, Anne L. Plant, Mary Brady, and Yaacov Yesha. "Image classification of vascular smooth muscle cells." In the ACM international conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1882992.1883068.

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Whitehead, Meredith, Sadia Ahmad, and Cathy Shanahan. "132 Role of vascular smooth muscle cell derived-exosomes in age-related vascular amyloidosis." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.129.

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Whitehead, Meredith, Sadia Ahmad, and Catherine Shanahan. "BS47 Role of vascular smooth muscle cell-derived exosomes in age-related vascular amyloidosis." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.208.

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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.

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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.
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Jover, Eva, Ana Silvente, Francisco Marín, Carmen María Puche, Mariano Valdés, Diana Hernández-Romero, José Martínez-González, Mar Orriols, Carlos Manuel Martinez, and Cristina Rodriguez. "115 Plods and lox participate in vascular smooth muscle cell calcification." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.114.

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