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Journal articles 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

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Shi, Zhenhua, Shiyong Ye, Yijia Xiang, Daying Wu, Jian Xu, Jianqiang Yu, Chunlai Zeng, Jun Jiang, and Wuming Hu. "circFAT1(e2) Inhibits Cell Apoptosis and Facilitates Progression in Vascular Smooth Muscle Cells through miR-298/MYB Axis." Computational and Mathematical Methods in Medicine 2021 (December 13, 2021): 1–11. http://dx.doi.org/10.1155/2021/1922366.

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Presently, as one of the three types of muscles in the human body, smooth muscle carries out many biological activities. Meanwhile, its abnormal development also leads to many diseases. Circular RNA, belonging to the noncoding RNA family, is demonstrated to function importantly in various diseases including smooth muscle. Here, we assumed circFAT1(e2) probably exhibited a primary role in vascular smooth muscle. Therefore, we conducted cell viability and cell apoptosis assay to validate the effects of circFAT1(e2) on vascular smooth muscle progression. Then, we supposed miR-298 was one target of circFAT1(e2) and executed corresponding experiments to test this hypothesis. Dual-luciferase reporter assay indicated miR-298 could bind to circFAT1(e2) and then modulated MYB level, thus regulating smooth muscle progression. Subsequently, based on the GSE41177 dataset, we identified 1982 differentially expressed genes (DEGs) in atrial fibrillation, and all DEGs were upregulated, including MYB. Finally, enrichment analysis of upregulated genes indicated that they were related to endodermal cell differentiation. The protein-protein interaction network revealed that EGFR, GNG2, and FPR2 were related to atrial fibrillation. In conclusion, our data find that circFAT1(e2) sponges miR-298 and then regulates MYB expression, thus affecting atrial fibrillation progression. Our findings provide a newly produced indicator and target for vascular smooth muscle diagnosis and treatment.
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12

NAITO, Michitaka, Kanichi ASAI, Kazuaki SHIBATA, Masafumi KUZUYA, Chiaki FUNAKI, and Fumio KUZUYA. "Vascular Endothelial and Smooth Muscle Cell Migration." Journal of Japan Atherosclerosis Society 13, no. 5 (1985): 1177–78. http://dx.doi.org/10.5551/jat1973.13.5_1177.

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13

Anfinogenova, Y. J., A. A. Kilin, I. V. Kovalev, M. B. Baskakov, N. O. Dulin, and S. N. Orlov. "CELL SHRINKAGE-INDUCED VASCULAR SMOOTH MUSCLE CONTRACTION." Journal of Hypertension 22, Suppl. 2 (June 2004): S44—S45. http://dx.doi.org/10.1097/00004872-200406002-00147.

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14

Hixon, Mary L., Carlos Obejero-Paz, Carlos Muro-Cacho, Mark W. Wagner, Elise Millie, Joanna Nagy, Terry J. Hassold, and Antonio Gualberto. "Cks1 Mediates Vascular Smooth Muscle Cell Polyploidization." Journal of Biological Chemistry 275, no. 51 (September 25, 2000): 40434–42. http://dx.doi.org/10.1074/jbc.m005059200.

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15

Morrow, David, Shaunta Guha, Catherine Sweeney, Yvonne Birney, Tony Walshe, Colm O’Brien, Dermot Walls, Eileen M. Redmond, and Paul A. Cahill. "Notch and Vascular Smooth Muscle Cell Phenotype." Circulation Research 103, no. 12 (December 5, 2008): 1370–82. http://dx.doi.org/10.1161/circresaha.108.187534.

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16

Weissberg, P. L., G. J. Clesham, and M. R. Bennett. "Is vascular smooth muscle cell proliferation beneficial?" Lancet 347, no. 8997 (February 1996): 305–7. http://dx.doi.org/10.1016/s0140-6736(96)90472-9.

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17

Rzucidlo, Eva M., Kathleen A. Martin, and Richard J. Powell. "Regulation of vascular smooth muscle cell differentiation." Journal of Vascular Surgery 45, no. 6 (June 2007): A25—A32. http://dx.doi.org/10.1016/j.jvs.2007.03.001.

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18

GORENNE, I., M. KAVURMA, S. SCOTT, and M. BENNETT. "Vascular smooth muscle cell senescence in atherosclerosis." Cardiovascular Research 72, no. 1 (October 1, 2006): 9–17. http://dx.doi.org/10.1016/j.cardiores.2006.06.004.

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19

Chang, Woochul, Soyeon Lim, Heesang Song, Byeong-Wook Song, Hye-Jung Kim, Min-Ji Cha, Jae Mo Sung, Tae Woong Kim, and Ki-Chul Hwang. "Cordycepin inhibits vascular smooth muscle cell proliferation." European Journal of Pharmacology 597, no. 1-3 (November 2008): 64–69. http://dx.doi.org/10.1016/j.ejphar.2008.08.030.

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20

Sung, Cheng-Po, Anthony J. Arleth, and Eliot H. Ohlstein. "Carvedilol Inhibits Vascular Smooth Muscle Cell Proliferation." Journal of Cardiovascular Pharmacology 21, no. 2 (February 1993): 221–27. http://dx.doi.org/10.1097/00005344-199302000-00006.

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21

Marx, Steven O., Hana Totary-Jain, and Andrew R. Marks. "Vascular Smooth Muscle Cell Proliferation in Restenosis." Circulation: Cardiovascular Interventions 4, no. 1 (February 2011): 104–11. http://dx.doi.org/10.1161/circinterventions.110.957332.

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22

Furmanik, G., M. Chatrou, B. Willems, R. van Gorp, H. Schmidt, G. van Eys, M. L. Bochaton-Piallat, et al. "Nox5 Regulates Vascular Smooth Muscle Cell Phenotype." Atherosclerosis 287 (August 2019): e27. http://dx.doi.org/10.1016/j.atherosclerosis.2019.06.079.

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23

Taylor, Angela M., and Coleen A. McNamara. "Regulation of Vascular Smooth Muscle Cell Growth." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 10 (October 2003): 1717–20. http://dx.doi.org/10.1161/01.atv.0000094396.24766.dd.

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24

Poon, M., S. O. Marx, R. Gallo, J. J. Badimon, M. B. Taubman, and A. R. Marks. "Rapamycin inhibits vascular smooth muscle cell migration." Journal of Clinical Investigation 98, no. 10 (November 15, 1996): 2277–83. http://dx.doi.org/10.1172/jci119038.

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25

Boyle, Joseph J. "Vascular smooth muscle cell apoptosis in atherosclerosis." International Journal of Experimental Pathology 80, no. 4 (December 25, 2001): 197–203. http://dx.doi.org/10.1046/j.1365-2613.1999.00125.x.

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26

Wada, Takeo, Marc D. McKee, Susie Steitz, and Cecilia M. Giachelli. "Calcification of Vascular Smooth Muscle Cell Cultures." Circulation Research 84, no. 2 (February 5, 1999): 166–78. http://dx.doi.org/10.1161/01.res.84.2.166.

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27

Bai, Hong-zhi, Matthew J. Pollman, Yoji Inishi, and Gary H. Gibbons. "Regulation of Vascular Smooth Muscle Cell Apoptosis." Circulation Research 85, no. 3 (August 6, 1999): 229–37. http://dx.doi.org/10.1161/01.res.85.3.229.

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28

Mehrhof, Felix B., Ruth Schmidt-Ullrich, Rainer Dietz, and Claus Scheidereit. "Regulation of Vascular Smooth Muscle Cell Proliferation." Circulation Research 96, no. 9 (May 13, 2005): 958–64. http://dx.doi.org/10.1161/01.res.0000166924.31219.49.

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29

Gerthoffer, William T. "Mechanisms of Vascular Smooth Muscle Cell Migration." Circulation Research 100, no. 5 (March 16, 2007): 607–21. http://dx.doi.org/10.1161/01.res.0000258492.96097.47.

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30

Reil, Todd D., Rajabrata Sarkar, Vikram S. Kashyap, Minakshi Sarkar, and Hugh A. Gelabert. "Dexamethasone Suppresses Vascular Smooth Muscle Cell Proliferation." Journal of Surgical Research 85, no. 1 (July 1999): 109–14. http://dx.doi.org/10.1006/jsre.1999.5665.

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31

Ghoneim, Shams, Zsuzsa Fabry, Judy Keiner, and Michael Hart. "Behavior and Cell-to-Cell Interaction of Cultured Endothelia and Smooth Muscle Cells Seeded on Nucleopore Filter." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 160–61. http://dx.doi.org/10.1017/s0424820100158340.

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Vascular endothelia and smooth muscle cultures, derived from small vessels may retain some of their in vivo characteristics. It has been demonstrated by other investigators that there exists in-vivo a close relationship between endothelia cells and smooth muscle cells of most vascular beds. The myo-endothelial junction has functional implications which could explain a humoral transmition of substances between the two cell population. Rhodin demonstrated that arteriolar endothelium exhibited foot-like processes which penetrated the endothelial basement membrane and extended into smooth muscle cells of the media(1). Fawcett, believed that a pathway exists between endothelia and smooth muscle cells for the exchange of metabolites (2).The objective of this in-vitro study was to examine the possible relationship between smooth muscle and endothelia cells in culture. Nucleopore filters with both 0.4μ and 3.0μ pores were used. They were seeded for 6 days with mouse brain endothelia cells on the top side of the filter and for 7 days with smooth muscle cells on the bottom side.
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32

Stephenson, Makeda, Daniel H. Reich, and Kenneth R. Boheler. "Induced pluripotent stem cell-derived vascular smooth muscle cells." Vascular Biology 2, no. 1 (January 9, 2020): R1—R15. http://dx.doi.org/10.1530/vb-19-0028.

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The reproducible generation of human-induced pluripotent stem cell (hiPSC)-derived vascular smooth muscle cells (vSMCs) in vitro has been critical to overcoming many limitations of animal and primary cell models of vascular biology and disease. Since this initial advance, research in the field has turned toward recapitulating the naturally occurring subtype specificity found in vSMCs throughout the body, and honing functional models of vascular disease. In this review, we summarize vSMC derivation approaches, including current phenotype and developmental origin-specific methods, and applications of vSMCs in functional disease models and engineered tissues. Further, we discuss the challenges of heterogeneity in hiPSC-derived tissues and propose approaches to identify and isolate vSMC subtype populations.
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33

Herbert, Jean-Marc, and Jean-Pierre Maffrand. "Heparin interactions with cultured human vascular endothelial and smooth muscle cells: Incidence on vascular smooth muscle cell proliferation." Journal of Cellular Physiology 138, no. 2 (February 1989): 424–32. http://dx.doi.org/10.1002/jcp.1041380226.

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34

Orlandi, Augusto, and Martin Bennett. "Progenitor cell-derived smooth muscle cells in vascular disease." Biochemical Pharmacology 79, no. 12 (June 2010): 1706–13. http://dx.doi.org/10.1016/j.bcp.2010.01.027.

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35

Luo, Y., P. A. D'Amore, and M. E. Dorf. "Beta-chemokine TCA3 binds to and activates rat vascular smooth muscle cells." Journal of Immunology 157, no. 5 (September 1, 1996): 2143–48. http://dx.doi.org/10.4049/jimmunol.157.5.2143.

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Abstract The present study compares the activity of TCA3 with other beta-chemokines (macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, and monocyte chemoattractant protein (MCP)-1) on rat vascular smooth muscle cells. TCA3, MIP-1 alpha, and MCP-1 (but not MIP-1 beta) treatment stimulates chemotaxis of vascular smooth muscle cells. TCA3-mediated chemotactic responses are sensitive to treatment with pertussis toxin, suggesting that G alpha-i proteins are involved in TCA3 signaling of smooth muscle. In addition, TCA3, MIP-1 alpha, and MCP-1 increase vascular smooth muscle cell adhesiveness to type III collagen. In contrast, stimulation with TCA3, but not other beta-chemokines, induces proliferation of vascular smooth muscle cells. TCA3 receptors were identified on rat vascular smooth muscle cells by direct binding of radiolabeled ligand. TCA3 binds to this receptor with high affinity (3 nM). Rat vascular smooth muscle cells display approximately 75,000 binding sites/cell. Competitive inhibition studies indicated that murine MIP-1 alpha, murine MCP-1, and human RANTES are weak partial competitors of TCA3 binding, demonstrating the existence of a unique receptor for TCA3. Murine MIP-1 beta, which fails to stimulate any biologic functions in vascular smooth muscle cells, also does not inhibit TCA3 binding. The combined data demonstrate that TCA3 and other beta-chemokines can modulate vascular smooth muscle cell function.
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36

Sehgel, Nancy L., Yi Zhu, Zhe Sun, Jerome P. Trzeciakowski, Zhongkui Hong, William C. Hunter, Dorothy E. Vatner, Gerald A. Meininger, and Stephen F. Vatner. "Increased vascular smooth muscle cell stiffness: a novel mechanism for aortic stiffness in hypertension." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 9 (November 1, 2013): H1281—H1287. http://dx.doi.org/10.1152/ajpheart.00232.2013.

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Increased vascular stiffness is fundamental to hypertension, and its complications, including atherosclerosis, suggest that therapy should also be directed at vascular stiffness, rather than just the regulation of peripheral vascular resistance. It is currently held that the underlying mechanisms of vascular stiffness in hypertension only involve the extracellular matrix and endothelium. We hypothesized that increased large-artery stiffness in hypertension is partly due to intrinsic mechanical properties of vascular smooth muscle cells. After confirming increased arterial pressure and aortic stiffness in spontaneously hypertensive rats, we found increased elastic stiffness of aortic smooth muscle cells of spontaneously hypertensive rats compared with Wistar-Kyoto normotensive controls using both an engineered aortic tissue model and atomic force microscopy nanoindentation. Additionally, we observed different temporal oscillations in the stiffness of vascular smooth muscle cells derived from hypertensive and control rats, suggesting that a dynamic component to cellular elastic stiffness is altered in hypertension. Treatment with inhibitors of vascular smooth muscle cell cytoskeletal proteins reduced vascular smooth muscle cell stiffness from hypertensive and control rats, suggesting their participation in the mechanism. This is the first study demonstrating that stiffness of individual vascular smooth muscle cells mediates vascular stiffness in hypertension, a novel concept, which may elucidate new therapies for hypertension and for vascular stiffness.
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37

Berk, Bradford C. "Vascular Smooth Muscle Growth: Autocrine Growth Mechanisms." Physiological Reviews 81, no. 3 (July 1, 2001): 999–1030. http://dx.doi.org/10.1152/physrev.2001.81.3.999.

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Vascular smooth muscle cells (VSMC) exhibit several growth responses to agonists that regulate their function including proliferation (hyperplasia with an increase in cell number), hypertrophy (an increase in cell size without change in DNA content), endoreduplication (an increase in DNA content and usually size), and apoptosis. Both autocrine growth mechanisms (in which the individual cell synthesizes and/or secretes a substance that stimulates that same cell type to undergo a growth response) and paracrine growth mechanisms (in which the individual cells responding to the growth factor synthesize and/or secrete a substance that stimulates neighboring cells of another cell type) are important in VSMC growth. In this review I discuss the autocrine and paracrine growth factors important for VSMC growth in culture and in vessels. Four mechanisms by which individual agonists signal are described: direct effects of agonists on their receptors, transactivation of tyrosine kinase-coupled receptors, generation of reactive oxygen species, and induction/secretion of other growth and survival factors. Additional growth effects mediated by changes in cell matrix are discussed. The temporal and spatial coordination of these events are shown to modulate the environment in which other growth factors initiate cell cycle events. Finally, the heterogeneous nature of VSMC developmental origin provides another level of complexity in VSMC growth mechanisms.
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38

Yamada, Hiroyuki, Masahiro Akishita, Masaaki Ito, Kouichi Tamura, Laurent Daviet, Jukka Y. A. Lehtonen, Victor J. Dzau, and Masatsugu Horiuchi. "AT2Receptor and Vascular Smooth Muscle Cell Differentiation in Vascular Development." Hypertension 33, no. 6 (June 1999): 1414–19. http://dx.doi.org/10.1161/01.hyp.33.6.1414.

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39

Uranishi, Ryunosuke, Nikolay I. Baev, Jung H. Kim, and Issam A. Awad. "Vascular Smooth Muscle Cell Differentiation in Human Cerebral Vascular Malformations." Neurosurgery 49, no. 3 (September 2001): 671–80. http://dx.doi.org/10.1227/00006123-200109000-00027.

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40

Shawer, H., K. Hemmings, N. Yuldasheva, K. Porter, R. Foster, R. Cubbon, J. Schneider, K. Griffin, D. Beech, and M. Bailey. "Vascular smooth muscle cell ORAI1 in vascular health and disease." Atherosclerosis 315 (December 2020): e31-e32. http://dx.doi.org/10.1016/j.atherosclerosis.2020.10.105.

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41

Uranishi, Ryunosuke, Nikolay I. Baev, Jung H. Kim, and Issam A. Awad. "Vascular Smooth Muscle Cell Differentiation in Human Cerebral Vascular Malformations." Neurosurgery 49, no. 3 (September 1, 2001): 671–80. http://dx.doi.org/10.1097/00006123-200109000-00027.

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42

Colucci, Wilson S., Tommy A. Brock, William J. Atkinson, R. Wayne Alexander, and Michael A. Gimbrone. "Cultured Vascular Smooth Muscle Cells." Journal of Cardiovascular Pharmacology 7 (1985): S79—S86. http://dx.doi.org/10.1097/00005344-198500076-00014.

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43

Capponi, Alessandro M., P. Daniel Lew, and Michel B. Vallotton. "Cultured Vascular Smooth Muscle Cells." Journal of Cardiovascular Pharmacology 8 (1986): S136—S138. http://dx.doi.org/10.1097/00005344-198600088-00027.

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44

Majesky, Mark W., Xiu Rong Dong, Jenna N. Regan, and Virginia J. Hoglund. "Vascular Smooth Muscle Progenitor Cells." Circulation Research 108, no. 3 (February 4, 2011): 365–77. http://dx.doi.org/10.1161/circresaha.110.223800.

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45

Yan, Zhong-Qun, Xintong Jiang, and Göran K. K. Hansson. "NOD1-high Vascular Smooth Muscle Cells are Vascular Resident Innate Immune Cell." Atherosclerosis Supplements 32 (June 2018): 114. http://dx.doi.org/10.1016/j.atherosclerosissup.2018.04.351.

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46

Wehbe, Nadine, Suzanne Awni Nasser, Yusra Al-Dhaheri, Rabah Iratni, Alessandra Bitto, Ahmed F. El-Yazbi, Adnan Badran, Firas Kobeissy, Elias Baydoun, and Ali H. Eid. "EPAC in Vascular Smooth Muscle Cells." International Journal of Molecular Sciences 21, no. 14 (July 21, 2020): 5160. http://dx.doi.org/10.3390/ijms21145160.

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Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EPACs) have been shown to play vital roles in a plethora of pathways in different cell systems. While extensive research to identify the role of EPAC in the vasculature has been conducted, much remains to be explored to resolve the reported discordance in EPAC’s effects. In this paper, we review the role of EPAC in VSMCs, namely its regulation of the vascular tone and phenotypic switching, with the likely involvement of reactive oxygen species (ROS) in the interplay between EPAC and its targets/effectors.
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47

Ahmed, Sultan, and Derek T. Warren. "Vascular smooth muscle cell contractile function and mechanotransduction." Vessel Plus 2, no. 11 (November 5, 2018): 36. http://dx.doi.org/10.20517/2574-1209.2018.51.

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48

Regnault, Veronique, Alexandre Raoul, Celia Schellenberg, and Patrick Lacolley. "Smooth Muscle Cell Molecular Underpinnings of Vascular Ageing." Heart, Lung and Circulation 30, no. 11 (November 2021): 1595–98. http://dx.doi.org/10.1016/j.hlc.2021.09.002.

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49

Qi, Lihua, Wei Kong, and Yi Fu. "Vascular Smooth Muscle Cell Development and Cardiovascular Malformations." Cardiology Discovery 1, no. 4 (September 13, 2021): 259–68. http://dx.doi.org/10.1097/cd9.0000000000000035.

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Katsuda, Shogo, and Yoshikatsu Okada. "Vascular Smooth Muscle Cell Migration and Extracellular Matrix." Journal of Atherosclerosis and Thrombosis 1, Supplemment1 (1994): S34—S38. http://dx.doi.org/10.5551/jat1994.1.supplemment1_s34.

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