Journal articles: '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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Fager, Gunnar, Göran K. Hansson, Pia Ottosson, Björn Dahllöf, and Göran Bondjers. "Human arterial smooth muscle cells in culture." Experimental Cell Research 176, no. 2 (June 1988): 319–35. http://dx.doi.org/10.1016/0014-4827(88)90334-5.

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Majesky, Mark W., and Stephen M. Schwartz. "Smooth Muscle Diversity in Arterial Wound Repair*." Toxicologic Pathology 18, no. 4a (January 1990): 554–59. http://dx.doi.org/10.1177/019262339001804a05.

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Repair of arterial injury results in formation of a new structure, a neointima, that causes luminal narrowing. Smooth muscle cell (SMC) properties required for neointima formation are also found in nascent SMCs of developing blood vessels in the embryo (e.g., proliferation, extracellular matrix synthesis, cell migration). We isolated 2 distinct types of SMC from aortic media of newborn rats that were distinguished by cell shape, secretion of platelet-derived growth factor (PDGF) and insulin-like growth factor-1 (IGF-1), and expression of PDGF-B and PDGF α-receptor genes. These two SMC types did not interconvert over many cell generations in vitro. Adult rat aorta yields only one SMC type, suggesting that the “pup” SMC variant is developmentally regulated. However, SMC with the “pup” phenotype reappear in the adult artery wall during neointima formation after balloon catheter injury. These observations raise the possibility that SMC proliferation and arterial remodeling during development, repair and disease of the artery wall might depend upon a SMC subpopulation with special properties.

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Oikawa, S., K. Hayasaka, E. Hashizume, H. Kotake, H. Midorikawa, A. Sekikawa, A. Kikuchi, and T. Toyota. "Human Arterial Smooth Muscle Cell Proliferation in Diabetes." Diabetes 45, Supplement_3 (July 1, 1996): S114—S116. http://dx.doi.org/10.2337/diab.45.3.s114.

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14

REIDY, MICHAEL A. "Growth Factors and Arterial Smooth Muscle Cell Proliferationa." Annals of the New York Academy of Sciences 714, no. 1 (April 1994): 225–30. http://dx.doi.org/10.1111/j.1749-6632.1994.tb12047.x.

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Chobanian, Aram V. "The arterial smooth muscle cell in systemic hypertension." American Journal of Cardiology 60, no. 17 (December 1987): 94–98. http://dx.doi.org/10.1016/0002-9149(87)90467-x.

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Macdonald, R. L., B. K. A. Weir, M. G. A. Grace, M. H. Chen, T. P. Martin, and J. D. Young. "Mechanism of Cerebral Vasospasm Following Subarachnoid Hemorrhage in Monkeys." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 4 (November 1992): 419–27. http://dx.doi.org/10.1017/s0317167100041597.

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ABSTRACT:This paper reviews our recent studies on the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH) in monkeys. Middle cerebral artery (MCA) vasospasm was maximal at 7 days, resolving by 14 days, and absent at 28 days after SAH. Arterial fibrosis was not detected during vasospasm, although there was intimal hyperplasia with fibrosis 28 days after SAH. On scanning electron microscopy, smooth muscle cells from vasospastic arteries had corrugated cell membranes and appeared similar to cells contracted pharmacologically, suggesting that vasospastic smooth muscle is contracted. Morphometric analysis of arteries obtained 7 days after SAH showed no significant increases in arterial wall area of vasospastic arteries compared with normal MCAs. The results suggest vasospasm in monkeys is not due to hypertrophy, hyperplasia, or fibrosis in the arterial wall. Vasospasm may be mainly vascular smooth muscle contraction, which damages the arterial wall, leading to secondary structural changes in the arterial wall which occur after angiographic vasospasm.

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Fujii, Satoshi, and Kazuhiko Fujitsu. "Experimental vasospasm in cultured arterial smooth-muscle cells." Journal of Neurosurgery 69, no. 1 (July 1988): 92–97. http://dx.doi.org/10.3171/jns.1988.69.1.0092.

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✓ Smooth-muscle cells were cultured from rat aortic media, then oxyhemoglobin and other agents including serotonin, norepinephrine, and angiotensin II were added separately to the medium. Contractile and ultrastructural changes of the cells were examined with electron microscopy during the first 2 weeks of incubation. Oxyhemoglobin not only produced progressive contraction of the arterial smooth-muscle cells, but it also caused ultrastructural changes that resembled myonecrosis. In contrast, there was no evidence of progressive contraction or ultrastructural changes either in control cultures or in cultures with the other vasoactive agents. Although washout of oxyhemoglobin 3 hours after administration prevented continued contraction of the cells, washout 24 hours or longer after administration had no preventive effect. Judging from these results and from the fact that the culture medium was changed every 2 days, it is unlikely that accumulation of exogenous vasoactive agents caused these changes. The contraction and suggestive myonecrosis of the arterial smooth-muscle cells are probably caused by some intrinsic process initiated by oxyhemoglobin. The culture of cerebral arterial smooth-muscle cells requires further technical improvement; nevertheless, these results obtained with the smooth-muscle cells of rat aortic media indicate that arterial smooth-muscle cells in culture provide a promising new experimental model for chronic in vitro study of cerebral arterial spasm. It is suggested from these results that cerebral arteries are particularly prone to vasospasm because of structural differences as compared to noncerebral arteries.

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Schmidt, Annette, and Eckhart Buddecke. "Cell-associated proteoheparan sulfate from bovine arterial smooth muscle cells." Experimental Cell Research 178, no. 2 (October 1988): 242–53. http://dx.doi.org/10.1016/0014-4827(88)90395-3.

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Löhn, Matthias, Dietmar Kämpf, Chai Gui-Xuan, Hermann Haller, Friedrich C. Luft, and Maik Gollasch. "Regulation of arterial tone by smooth muscle myosin type II." American Journal of Physiology-Cell Physiology 283, no. 5 (November 1, 2002): C1383—C1389. http://dx.doi.org/10.1152/ajpcell.01369.2000.

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The initiation of contractile force in arterial smooth muscle (SM) is believed to be regulated by the intracellular Ca2+concentration and SM myosin type II phosphorylation. We tested the hypothesis that SM myosin type II operates as a molecular motor protein in electromechanical, but not in protein kinase C (PKC)-induced, contraction of small resistance-sized cerebral arteries. We utilized a SM type II myosin heavy chain (MHC) knockout mouse model and measured arterial wall Ca2+ concentration ([Ca2+]i) and the diameter of pressurized cerebral arteries (30–100 μm) by means of digital fluorescence video imaging. Intravasal pressure elevation caused a graded [Ca2+]i increase and constricted cerebral arteries of neonatal wild-type mice by 20–30%. In contrast, intravasal pressure elevation caused a graded increase of [Ca2+]i without constriction in (−/−) MHC-deficient arteries. KCl (60 mM) induced a further [Ca2+]i increase but failed to induce vasoconstriction of (−/−) MHC-deficient cerebral arteries. Activation of PKC by phorbol ester (phorbol 12-myristate 13-acetate, 100 nM) induced a strong, sustained constriction of (−/−) MHC-deficient cerebral arteries without changing [Ca2+]i. These results demonstrate a major role for SM type II myosin in the development of myogenic tone and Ca2+-dependent constriction of resistance-sized cerebral arteries. In contrast, the sustained contractile response did not depend on myosin and intracellular Ca2+ but instead depended on PKC. We suggest that SM myosin type II operates as a molecular motor protein in the development of myogenic tone but not in pharmacomechanical coupling by PKC in cerebral arteries. Thus PKC-dependent phosphorylation of cytoskeletal proteins may be responsible for sustained contraction in vascular SM.

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Dixon, B. S., R. Breckon, J. Fortune, R. J. Vavrek, J. M. Stewart, R. Marzec-Calvert, and S. L. Linas. "Effects of kinins on cultured arterial smooth muscle." American Journal of Physiology-Cell Physiology 258, no. 2 (February 1, 1990): C299—C308. http://dx.doi.org/10.1152/ajpcell.1990.258.2.c299.

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The present study uses various kinin agonists and antagonists to examine the cellular mechanisms of bradykinin's actions on intracellular calcium, prostaglandins, and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cultured arterial smooth muscle cells (casmc) obtained from rat mesenteric arteries. Exposure to bradykinin produced a rapid release of calcium (peak less than or equal to 20 s) from intracellular stores and an increase in prostaglandin (PG) E2 and cAMP production in casmc. Compared with bradykinin, the bradykinin B1-agonist [des-Arg9]BK produced only a small increase in intracellular calcium. The bradykinin-mediated increase in intracellular calcium was competitively blocked by the B2 receptor antagonist [D-Arg-O-Hyp3-Thi5,8-D-Phe7]BK (B4307) but not the B1-antagonist ([des-Arg9-Leu8]BK). In addition, the similarity of the dose-response curves for the bradykinin-mediated increase in Ca2+, PGE2, and cAMP (half-maximal stimulation of 12, 11, and 13 nM, respectively) and the ability of the B2-antagonist (B4307) to block each of these effects of bradykinin suggest that all three effects are mediated by the same bradykinin (B2) receptor. Further studies revealed that increases in intracellular calcium are necessary for the bradykinin-mediated increase in PGE2 formation and the subsequent PGE2-dependent formation of cAMP. Taken together, these results suggest that bradykinin acts via a B2-receptor on arterial smooth muscle cells to release calcium from intracellular stores, leading to increases in PGE2 production and the PGE2-dependent activation of adenylate cyclase.

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YU, Kenneth C. W., and John C. L. MAMO. "Chylomicron-remnant-induced foam cell formation and cytotoxicity: a possible mechanism of cell death in atherosclerosis." Clinical Science 98, no. 2 (January 11, 2000): 183–92. http://dx.doi.org/10.1042/cs0980183.

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The effects of chylomicron remnants on cytoplasmic lipid loading and cell viability were assessed in cultures of human monocyte-derived macrophages and rabbit arterial smooth muscle cells. At a cholesterol concentration of 150 μg/ml, chylomicron remnants induced substantial cytoplasmic lipid loading of macrophages, but not of smooth muscle cells, within 6 h of exposure. Chylomicron remnants were found to be cytotoxic to macrophages and smooth muscle cells, although the latter were generally more resistant. Chylomicron remnants contained no detectable oxysterols (> 1 ng) and contained less non-esterified (‘free’) fatty acids than non-lipolysed nascent chylomicrons. Chylomicron-remnant-induced cytotoxicity appeared to be time- and dose-dependent. Macrophage and smooth muscle cell viability were inversely related to the production of superoxide free radicals and were significantly improved in the combined presence of superoxide dismutase and catalase. Collectively, our data suggest that, in macrophages, cell viability is compromised as a consequence of superoxide free radical production following uptake of chylomicron remnants. We would suggest that, in arterial smooth muscle cells, chylomicron-remnant-induced cell death also occurs as a consequence of superoxide free radical production. Our observations in the present study suggest that macrophage foam cells in atherosclerotic plaques might be derived from the cellular uptake of chylomicron remnants. Furthermore, arterial accumulation of chylomicron remnants might contribute to plaque destabilization as a consequence of cell death following superoxide free radical production by macrophages and smooth muscle cells.

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HAJJAR, DAVID P., AARON J. MARCUS, and KATHERINE A. HAJJAR. "Arterial Endothelial Cell-derived Eicosanoids Alter Cholesterol Metabolism in Arterial Smooth Muscle Cells." Annals of the New York Academy of Sciences 524, no. 1 Biology of th (April 1988): 411–13. http://dx.doi.org/10.1111/j.1749-6632.1988.tb38571.x.

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Malam-Souley, R., M. Campan, A. P. Gadeau, and C. Desgranges. "Exogenous ATP induces a limited cell cycle progression of arterial smooth muscle cells." American Journal of Physiology-Cell Physiology 264, no. 4 (April 1, 1993): C783—C788. http://dx.doi.org/10.1152/ajpcell.1993.264.4.c783.

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Because exogenous ATP is suspected to influence the proliferative process, its effects on the cell cycle progression of arterial smooth muscle cells were studied by investigating changes in the mRNA steady-state level of cell cycle-dependent genes. Stimulation of cultured quiescent smooth muscle cells by exogenous ATP induced chronological activation not only of immediate-early but also of delayed-early cell cycle-dependent genes, which were usually expressed after a mitogenic stimulation. In contrast, ATP did not increase late G1 gene mRNA level, demonstrating that this nucleotide induces a limited cell cycle progression of arterial smooth muscle cells through the G1 phase but is not able by itself to induce crossing over the G1-S boundary and consequently DNA synthesis. An increase in c-fos mRNA level was also induced by ADP but not by AMP or adenosine. Moreover, 2-methylthioadenosine 5'-triphosphate but not alpha, beta-methyleneadenosine 5'-triphosphate mediated this kind of response. Taken together, these results demonstrate that extracellular ATP induces the limited progression of arterial smooth muscle cells through the G1 phase via its fixation on P2 gamma receptors.

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Budel, Stéphane, Alexander Schuster, Nikos Stergiopoulos, Jean-Jacques Meister, and Jean-Louis Bény. "Role of smooth muscle cells on endothelial cell cytosolic free calcium in porcine coronary arteries." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (September 1, 2001): H1156—H1162. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1156.

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We tested the hypothesis that the cytosolic free calcium concentration in endothelial cells is under the influence of the smooth muscle cells in the coronary circulation. In the left descending branch of porcine coronary arteries, cytosolic free calcium concentration ([Ca2+]i) was estimated by determining the fluorescence ratio of two calcium probes, fluo 4 and fura red, in smooth muscle and endothelial cells using confocal microscopy. Acetylcholine and potassium, which act directly on smooth muscle cells to increase [Ca2+]i, were found to indirectly elevate [Ca2+]i in endothelial cells; in primary cultures of endothelial cells, neither stimulus affected [Ca2+]i, yet substance P increased the fluorescence ratio twofold. In response to acetylcholine and potassium, isometric tension developed by arterial strips with intact endothelium was attenuated by up to 22% ( P < 0.05) compared with strips without endothelium. These findings suggest that stimuli that increase smooth muscle [Ca2+]i can indirectly influence endothelial cell function in porcine coronary arteries. Such a pathway for negative feedback can moderate vasoconstriction and diminish the potential for vasospasm in the coronary circulation.

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Carmeliet, Peter, Lieve Moons, Mieke Dewerchin, Steven Rosenberg, Jean-Marc Herbert, Florea Lupu, and Désiré Collen. "Receptor-independent Role of Urokinase-Type Plasminogen Activator in Pericellular Plasmin and Matrix Metalloproteinase Proteolysis during Vascular Wound Healing in Mice." Journal of Cell Biology 140, no. 1 (January 12, 1998): 233–45. http://dx.doi.org/10.1083/jcb.140.1.233.

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It has been proposed that the urokinase receptor (u-PAR) is essential for the various biological roles of urokinase-type plasminogen activator (u-PA) in vivo, and that smooth muscle cells require u-PA for migration during arterial neointima formation. The present study was undertaken to evaluate the role of u-PAR during this process in mice with targeted disruption of the u-PAR gene (u-PAR−/−). Surprisingly, u-PAR deficiency did not affect arterial neointima formation, neointimal cell accumulation, or migration of smooth muscle cells. Indeed, topographic analysis of arterial wound healing after electric injury revealed that u-PAR−/− smooth muscle cells, originating from the uninjured borders, migrated over a similar distance and at a similar rate into the necrotic center of the wound as wild-type (u-PAR+/+) smooth muscle cells. In addition, u-PAR deficiency did not impair migration of wounded cultured smooth muscle cells in vitro. There were no genotypic differences in reendothelialization of the vascular wound. The minimal role of u-PAR in smooth muscle cell migration was not because of absent expression, since wild-type smooth muscle cells expressed u-PAR mRNA and functional receptor in vitro and in vivo. Pericellular plasmin proteolysis, evaluated by degradation of 125I-labeled fibrin and activation of zymogen matrix metalloproteinases, was similar for u-PAR−/− and u-PAR+/+ cells. Immunoelectron microscopy of injured arteries in vivo revealed that u-PA was bound on the cell surface of u-PAR+/+ cells, whereas it was present in the pericellular space around u-PAR−/− cells. Taken together, these results suggest that binding of u-PA to u-PAR is not required to provide sufficient pericellular u-PA–mediated plasmin proteolysis to allow cellular migration into a vascular wound.

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Iwata, Hiroshi, Masataka Sata, Ichiro Manabe, Katsuhito Fujiu, Makoto Kuro-o, and Ryozo Nagai. "Examination of smooth muscle cell lineage in arterial remodeling with smooth muscle specific marker: Smooth muscle myosin heavy chain." Vascular Pharmacology 45, no. 3 (September 2006): e103-e104. http://dx.doi.org/10.1016/j.vph.2006.08.284.

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Adam, L. P., J. R. Haeberle, and D. R. Hathaway. "Phosphorylation of caldesmon in arterial smooth muscle." Journal of Biological Chemistry 264, no. 13 (May 1989): 7698–703. http://dx.doi.org/10.1016/s0021-9258(18)83291-4.

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Neuville, Pascal, Marie-Luce Bochaton-Piallat, and Giulio Gabbiani. "Retinoids and Arterial Smooth Muscle Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 20, no. 8 (August 2000): 1882–88. http://dx.doi.org/10.1161/01.atv.20.8.1882.

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Woodley, N., and J. K. Barclay. "CULTURED ENDOTHELIAL CELL SECRETARY PRODUCTS RELAX ARTERIAL SMOOTH MUSCLE." Medicine & Science in Sports & Exercise 24, Supplement (May 1992): S28. http://dx.doi.org/10.1249/00005768-199205001-00167.

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Mathura, Rishi A., Sparkle Russell-Puleri, Limary M. Cancel, and John M. Tarbell. "Hydraulic Conductivity of Smooth Muscle Cell-Initiated Arterial Cocultures." Annals of Biomedical Engineering 44, no. 5 (August 12, 2015): 1721–33. http://dx.doi.org/10.1007/s10439-015-1421-5.

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Bochaton-Piallat, Marie-Luce, Patricia Ropraz, Françoise Gabbiani, and Giulio Gabbiani. "Phenotypic Heterogeneity of Rat Arterial Smooth Muscle Cell Clones." Arteriosclerosis, Thrombosis, and Vascular Biology 16, no. 6 (June 1996): 815–20. http://dx.doi.org/10.1161/01.atv.16.6.815.

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32

Lacolley, Patrick. "TARGETING VASCULAR SMOOTH MUSCLE CELL TO IMPROVE ARTERIAL STIFFNESS." Artery Research 20, no. C (2017): 45. http://dx.doi.org/10.1016/j.artres.2017.10.008.

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Morales-Quinones, Mariana, Francisco I. Ramirez-Perez, Christopher A. Foote, Thaysa Ghiarone, Larissa Ferreira-Santos, Maria Bloksgaard, Nicole Spencer, et al. "LIMK (LIM Kinase) Inhibition Prevents Vasoconstriction- and Hypertension-Induced Arterial Stiffening and Remodeling." Hypertension 76, no. 2 (August 2020): 393–403. http://dx.doi.org/10.1161/hypertensionaha.120.15203.

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Increased arterial stiffness and vascular remodeling precede and are consequences of hypertension. They also contribute to the development and progression of life-threatening cardiovascular diseases. Yet, there are currently no agents specifically aimed at preventing or treating arterial stiffening and remodeling. Previous research indicates that vascular smooth muscle actin polymerization participates in the initial stages of arterial stiffening and remodeling and that LIMK (LIM kinase) promotes F-actin formation and stabilization via cofilin phosphorylation and consequent inactivation. Herein, we hypothesize that LIMK inhibition is able to prevent vasoconstriction- and hypertension-associated arterial stiffening and inward remodeling. We found that small visceral arteries isolated from hypertensive subjects are stiffer and have greater cofilin phosphorylation than those from nonhypertensives. We also show that LIMK inhibition prevents arterial stiffening and inward remodeling in isolated human small visceral arteries exposed to prolonged vasoconstriction. Using cultured vascular smooth muscle cells, we determined that LIMK inhibition prevents vasoconstrictor agonists from increasing cofilin phosphorylation, F-actin volume, and cell cortex stiffness. We further show that localized LIMK inhibition prevents arteriolar inward remodeling in hypertensive mice. This indicates that hypertension is associated with increased vascular smooth muscle cofilin phosphorylation, cytoskeletal stress fiber formation, and heightened arterial stiffness. Our data further suggest that pharmacological inhibition of LIMK prevents vasoconstriction-induced arterial stiffening, in part, via reductions in vascular smooth muscle F-actin content and cellular stiffness. Accordingly, LIMK inhibition should represent a promising therapeutic means to stop the progression of arterial stiffening and remodeling in hypertension.

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34

Lu, Gui-Feng, Fei Geng, Li-Ping Deng, Da-Cen Lin, Yan-Zhen Huang, Su-Mei Lai, Yi-Chen Lin, Long-Xin Gui, James S. K. Sham, and Mo-Jun Lin. "Reduced CircSMOC1 Level Promotes Metabolic Reprogramming via PTBP1 (Polypyrimidine Tract-Binding Protein) and miR-329-3p in Pulmonary Arterial Hypertension Rats." Hypertension 79, no. 11 (November 2022): 2465–79. http://dx.doi.org/10.1161/hypertensionaha.122.19183.

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Background: Pulmonary arterial hypertension maintains rapid cell proliferation and vascular remodeling through metabolic reprogramming. Recent studies suggested that circRNAs play important role in pulmonary vascular remodeling and pulmonary arterial smooth muscle cells proliferation. However, the relationship between circRNA, cell proliferation, and metabolic reprogramming in pulmonary arterial hypertension has not been investigated. Methods: RNA-seq and qRT-PCR reveal the differential expression profile of circRNA in pulmonary arteries of pulmonary arterial hypertension rat models. Transfection was used to examine the effects of circSMOC1 on pulmonary artery smooth muscle cells, and the roles of circSMOC1 in vivo were investigated by adenoassociated virus. Mass spectrometry, RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assay were performed to investigate the signaling pathway of circSMOC1 regulating the metabolic reprogramming. Results: CircSMOC1 was significantly downregulated in pulmonary arteries of pulmonary arterial hypertension rats. CircSMOC1 knockdown promoted proliferation and migration and enhanced aerobic glycolysis of pulmonary artery smooth muscle cells. CircSMOC1 overexpression in vivo alleviates pulmonary vascular remodeling, right ventricular pressure, and right heart hypertrophy. In the nucleus, circSMOC1 directly binds to PTBP1 (polypyrimidine tract-binding protein), competitively inhibits the specific splicing of PKM (pyruvate kinase M) premRNA, resulting in the upregulation of PKM2 (pyruvate kinase M2), the key enzyme of aerobic glycolysis, to enhance glycolysis. In the cytoplasm, circSMOC1 acted as a miR-329-3p sponge, and its reduction in pulmonary arterial hypertension suppressed PDHB (pyruvate dehydrogenase E1 subunit beta) expression, leading to the impairment of mitochondrial oxidative phosphorylation. Conclusions: circSMOC1 is crucially involved in the metabolic reprogramming of pulmonary artery smooth muscle cells through PTBP1 and miR-329-3p to regulate pulmonary vascular remodeling in pulmonary arterial hypertension.

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35

Bowles, D. K., Q. Hu, M. H. Laughlin, and M. Sturek. "Exercise training increases L-type calcium current density in coronary smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 6 (December 1, 1998): H2159—H2169. http://dx.doi.org/10.1152/ajpheart.1998.275.6.h2159.

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Exercise training produces numerous adaptations in the coronary circulation, including an increase in coronary tone, both in conduit and resistance arteries. On the basis of the importance of voltage-gated Ca2+ channels (VGCC) in regulation of vascular tone, we hypothesized that exercise training would increase VGCC current density in coronary smooth muscle. To test this hypothesis, VGCC current was compared in smooth muscle from conduit arteries (>1.0 mm), small arteries (200–250 μm), and large arterioles (75–150 μm) from endurance-trained (Ex) or sedentary miniature swine (Sed). After 16–20 wk of treadmill training, VGCC current was determined using whole cell voltage-clamp techniques. In both Ex and Sed, VGCC current density was inversely related to arterial diameter, i.e., large arterioles > small arteries > conduit arteries. Exercise training increased peak inward currents approximately twofold in smooth muscle from all arterial sizes compared with those from Sed (large arteriole, −12.52 ± 2.05 vs. −5.74 ± 0.99 pA/pF; small artery, −6.20 ± 0.97 vs. −3.18 ± 0.44 pA/pF; and conduit arteries, −4.22 ± 0.30 vs. −2.41 ± 0.55 pA/pF; 10 mM Ba2+ external). Dihydropyridine sensitivity, voltage dependence, and inactivation kinetics identified this Ca2+ current to be L-type current in all arterial sizes from both Sed and Ex. Furthermore, peak VGCC current density was correlated with treadmill endurance in all arterial sizes. We conclude that smooth muscle L-type Ca2+ current density is increased within the coronary arterial bed by endurance exercise training. This increased VGCC density may provide an important mechanistic link between functional and cellular adaptations in the coronary circulation to exercise training.

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Wang, Shuang, Weiwei Cao, Shan Gao, Xiaowei Nie, Xiaodong Zheng, Yan Xing, Yingli Chen, Hongxia Bao, and Daling Zhu. "TUG1 Regulates Pulmonary Arterial Smooth Muscle Cell Proliferation in Pulmonary Arterial Hypertension." Canadian Journal of Cardiology 35, no. 11 (November 2019): 1534–45. http://dx.doi.org/10.1016/j.cjca.2019.07.630.

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Bialecki, R. A., and T. N. Tulenko. "Excess membrane cholesterol alters calcium channels in arterial smooth muscle." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C306—C314. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c306.

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We studied the effects of cholesterol enrichment on arterial function by evaluating its effects on 45Ca2+ uptake and tension development in the carotid artery of the rabbit. Arterial segments were enriched with cholesterol in vitro, using media containing liposomes composed of free (unesterified) cholesterol (FC) and phospholipid (PL) in a 2:1 molar ratio. Control segments were simultaneously perfused with 0.5:1 liposomal medium to compare the possible effects of PL. Rings from these arteries were then tested for basal and activated Ca2+ uptake and for contractile responses to norepinephrine (NE) and KCl. We found elevated 45Ca2+ uptake under basal and NE-activated conditions along with an increased contractile sensitivity (4-fold) to NE. These alterations correlated with a 78% increase in the FC/PL ratio reflecting cholesterol enrichment of cellular membranes. Cholesterol enrichment did not alter resting or maximal tensions, K+-activated Ca2+ uptake, or contractile sensitivity to K+. Pretreatment with 1 microM diltiazem abolished the cholesterol-induced increase in basal as well as NE-activated 45Ca2+ uptake but had no effect on either uptake in control vessels. These studies suggest that excess membrane cholesterol selectively increases NE contractile sensitivity by increasing basal or NE-activated Ca2+ influx (or both) as a result of fundamental alteration in the calcium channels in arterial smooth muscle cell membrane.

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Coppock, Elizabeth A., Jeffrey R. Martens, and Michael M. Tamkun. "Molecular basis of hypoxia-induced pulmonary vasoconstriction: role of voltage-gated K+ channels." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (July 1, 2001): L1—L12. http://dx.doi.org/10.1152/ajplung.2001.281.1.l1.

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The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of vascular smooth muscle cell voltage-gated K+(KV) channels open at the resting membrane potential. Pulmonary arterial smooth muscle cell KV channel expression, antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, and the O2 sensitivity of cloned KV channels expressed in heterologous expression systems have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive KV current. Likely components include Kv2.1/Kv9.3 and Kv1.2/Kv1.5 heteromeric channels and the Kv3.1b α-subunit. Although the mechanism of KV channel inhibition by hypoxia is unknown, it appears that KV α-subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or β-subunit. This review summarizes the role of KV channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of KV channel subunits involved in this response, and the possible mechanisms of KV channel regulation by hypoxia.

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Fang, X., M. VanRollins, T. L. Kaduce, and A. A. Spector. "Epoxyeicosatrienoic acid metabolism in arterial smooth muscle cells." Journal of Lipid Research 36, no. 6 (June 1995): 1236–46. http://dx.doi.org/10.1016/s0022-2275(20)41131-9.

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40

Han, Jin, Nari Kim, Hyun Joo, and Euiyong Kim. "Ketamine blocks Ca2+-activated K+ channels in rabbit cerebral arterial smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H1347—H1355. http://dx.doi.org/10.1152/ajpheart.00194.2003.

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Although ketamine and Ca2+-activated K+ (KCa) channels have been implicated in the contractile activity regulation of cerebral arteries, no studies have addressed the specific interactions between ketamine and the KCa channels in cerebral arteries. The purpose of this study was to examine the direct effects of ketamine on KCa channel activities using the patch-clamp technique in single-cell preparations of rabbit middle cerebral arterial smooth muscle. We tested the hypothesis that ketamine modulates the KCa channel activity of the cerebral arterial smooth muscle cells of the rabbit. Vascular myocytes were isolated from rabbit middle cerebral arteries using enzymatic dissociation. Single KCa channel activities of smooth muscle cells from rabbit cerebral arteries were recorded using the patch-clamp technique. In the inside-out patches, ketamine in the micromolar range inhibited channel activity with a half-maximal inhibition of the ketamine conentration value of 83.8 ± 12.9 μM. The Hill coefficient was 1.2 ± 0.3. The slope conductance of the current-voltage relationship was 320.1 ± 2.0 pS between 0 and +60 mV in the presence of ketamine and symmetrical 145 mM K+. Ketamine had little effect on either the voltage-dependency or open- and closed-time histograms of KCa channel. The present study clearly demonstrates that ketamine inhibits KCa channel activities in rabbit middle cerebral arterial smooth muscle cells. This inhibition of KCa channels may represent a mechanism for ketamine-induced cerebral vasoconstriction.

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Bannister, John P., Simon Bulley, M. Dennis Leo, Michael W. Kidd, and Jonathan H. Jaggar. "Rab25 influences functional Cav1.2 channel surface expression in arterial smooth muscle cells." American Journal of Physiology-Cell Physiology 310, no. 11 (June 1, 2016): C885—C893. http://dx.doi.org/10.1152/ajpcell.00345.2015.

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Plasma membrane-localized CaV1.2 channels are the primary calcium (Ca2+) influx pathway in arterial smooth muscle cells (myocytes). CaV1.2 channels regulate several cellular functions, including contractility and gene expression, but the trafficking pathways that control the surface expression of these proteins are unclear. Similarly, expression and physiological functions of small Rab GTPases, proteins that control vesicular trafficking in arterial myocytes, are poorly understood. Here, we investigated Rab proteins that control functional surface abundance of CaV1.2 channels in cerebral artery myocytes. Western blotting indicated that Rab25, a GTPase previously associated with apical recycling endosomes, is expressed in cerebral artery myocytes. Immunofluorescence Förster resonance energy transfer (immunoFRET) microscopy demonstrated that Rab25 locates in close spatial proximity to CaV1.2 channels in myocytes. Rab25 knockdown using siRNA reduced CaV1.2 surface and intracellular abundance in arteries, as determined using arterial biotinylation. In contrast, CaV1.2 was not located nearby Rab11A or Rab4 and CaV1.2 protein was unaltered by Rab11A or Rab4A knockdown. Rab25 knockdown resulted in CaV1.2 degradation by a mechanism involving both lysosomal and proteasomal pathways and reduced whole cell CaV1.2 current density but did not alter voltage dependence of current activation or inactivation in isolated myocytes. Rab25 knockdown also inhibited depolarization (20–60 mM K+) and pressure-induced vasoconstriction (myogenic tone) in cerebral arteries. These data indicate that Rab25 is expressed in arterial myocytes where it promotes surface expression of CaV1.2 channels to control pressure- and depolarization-induced vasoconstriction.

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Lacolley, Patrick, Véronique Regnault, Patrick Segers, and Stéphane Laurent. "Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease." Physiological Reviews 97, no. 4 (October 1, 2017): 1555–617. http://dx.doi.org/10.1152/physrev.00003.2017.

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The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.

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Amberg, Gregory C., Charles F. Rossow, Manuel F. Navedo, and Luis F. Santana. "NFATc3 Regulates Kv2.1 Expression in Arterial Smooth Muscle." Journal of Biological Chemistry 279, no. 45 (August 22, 2004): 47326–34. http://dx.doi.org/10.1074/jbc.m408789200.

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Jantzi, Micaela C., Suzanne E. Brett, William F. Jackson, Randolph Corteling, Edward J. Vigmond, and Donald G. Welsh. "Inward rectifying potassium channels facilitate cell-to-cell communication in hamster retractor muscle feed arteries." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (September 2006): H1319—H1328. http://dx.doi.org/10.1152/ajpheart.00217.2006.

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This study examined whether inward rectifying K+(KIR) channels facilitate cell-to-cell communication along skeletal muscle resistance arteries. With the use of feed arteries from the hamster retractor muscle, experiments examined whether KIRchannels were functionally expressed and whether channel blockade attenuated the conduction of acetylcholine-induced vasodilation, an index of cell-to-cell communication. Consistent with KIRchannel expression, this study observed the following: 1) a sustained Ba2+-sensitive, K+-induced dilation in preconstricted arteries; 2) a Ba2+-sensitive inwardly rectifying K+current in arterial smooth muscle cells; and 3) KIR2.1 and KIR2.2 expression in the smooth muscle layer of these arteries. It was subsequently shown that the discrete application of acetylcholine elicits a vasodilation that conducts with limited decay along the feed artery wall. In the presence of 100 μM Ba2+, the local and conducted response to acetylcholine was attenuated, a finding consistent with a role for KIRin facilitating cell-to-cell communication. A computational model of vascular communication accurately predicted these observations. Control experiments revealed that in contrast to Ba2+, ATP-sensitive- and large-conductance Ca2+activated-K+channel inhibitors had no effect on the local or conducted vasodilatory response to acetylcholine. We conclude that smooth muscle KIRchannels play a key role in facilitating cell-to-cell communication along skeletal muscle resistance arteries. We attribute this facilitation to the intrinsic property of negative slope conductance, a biophysical feature common to KIR2.1- and 2.2-containing channels, which enables them to increase their activity as a cell hyperpolarizes.

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Jaggar, Jonathan H., Andrá S. Stevenson, and Mark T. Nelson. "Voltage dependence of Ca2+sparks in intact cerebral arteries." American Journal of Physiology-Cell Physiology 274, no. 6 (June 1, 1998): C1755—C1761. http://dx.doi.org/10.1152/ajpcell.1998.274.6.c1755.

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Ca2+ sparks have been previously described in isolated smooth muscle cells. Here we present the first measurements of local Ca2+ transients (“Ca2+ sparks”) in an intact smooth muscle preparation. Ca2+sparks appear to result from the opening of ryanodine-sensitive Ca2+ release (RyR) channels in the sarcoplasmic reticulum (SR). Intracellular Ca2+ concentration ([Ca2+]i) was measured in intact cerebral arteries (40–150 μm in diameter) from rats, using the fluorescent Ca2+ indicator fluo 3 and a laser scanning confocal microscope. Membrane potential depolarization by elevation of external K+ from 6 to 30 mM increased Ca2+ spark frequency (4.3-fold) and amplitude (∼2-fold) as well as global arterial wall [Ca2+]i(∼1.7-fold). The half time of decay (∼50 ms) was not affected by membrane potential depolarization. Ryanodine (10 μM), which inhibits RyR channels and Ca2+ sparks in isolated cells, and thapsigargin (100 nM), which indirectly inhibits RyR channels by blocking the SR Ca2+-ATPase, completely inhibited Ca2+ sparks in intact cerebral arteries. Diltiazem, an inhibitor of voltage-dependent Ca2+ channels, lowered global [Ca2+]iand Ca2+ spark frequency and amplitude in intact cerebral arteries in a concentration-dependent manner. The frequency of Ca2+sparks (<1 s−1 ⋅ cell−1), even under conditions of steady depolarization, was too low to contribute significant amounts of Ca2+ to global Ca2+ in intact arteries. These results provide direct evidence that Ca2+ sparks exist in quiescent smooth muscle cells in intact arteries and that changes of membrane potential that would simulate physiological changes modulate both Ca2+ spark frequency and amplitude in arterial smooth muscle.

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Wang, Deng, Dan Lai, and Chengfu Peng. "TWIST1 silencing attenuates intracranial aneurysms by inhibiting NF-κB signaling." Tropical Journal of Pharmaceutical Research 21, no. 5 (June 16, 2022): 927–32. http://dx.doi.org/10.4314/tjpr.v21i5.3.

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Purpose: To investigate the effect of Twist family basic helix-loop-helix transcription factor 1 (TWIST1) on intracranial aneurysms.Methods: A rat model of intracranial aneurysm was established by ligating the posterior branches of both the renal and left common carotid arteries. Pathological changes in the intracranial arterial wall were investigated using hematoxylin-eosin staining. TWIST1 expression was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot, while vascular smooth muscle cell apoptosis was investigated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Inflammation was evaluated using enzyme-linked immunosorbent assay (ELISA).Results: Rats with intracranial aneurysms had degenerative changes in vessel wall structure. Inintracranial aneurysm rats, TWIST1 was upregulated in arterial wall sections, and TWIST1 knockdown ameliorated the pathological changes to the arterial wall. TWIST1 silencing reduced serum tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels and suppressed vascular smooth muscle cell apoptosis in rats with intracranial aneurysms. TWIST1 knockdown increased phospho (p)-inhibitor of nuclear factor-κB (IκB) and decreased IκB and p-p65 in intracranial aneurysm rat arterial wall sections.Conclusion: In intracranial aneurysms, silencing TWIST1 promoted vascular remodeling and suppresses vascular smooth muscle cell apoptosis and inflammation through inactivating NF-κBsignaling, revealing TWIST1 silencing as a potential treatment strategy.

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Lee, Robert M. K. W., Gary K. Owens, Timothy Scott-Burden, Richard J. Head, Michael J. Mulvany, and Ernesto L. Schiffrin. "Pathophysiology of smooth muscle in hypertension." Canadian Journal of Physiology and Pharmacology 73, no. 5 (May 1, 1995): 574–84. http://dx.doi.org/10.1139/y95-073.

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Structural changes of the arteries in hypertension are determined by the unique genetics of the animals and by various growth promoters and growth inhibitors. Vascular smooth muscle cell growth promoting factors include fibroblast growth factor, platelet-derived growth factor, and vasoactive peptides such as norepinephrine, angiotensin II, and endothelin. Endothelial cells secrete three types of growth inhibiting factors. These are heparin – heparan sulfate, transforming growth factor β, and nitric oxide. The effect of sympathetic innervation on vascular growth is probably dependent on its interaction with the rennin–angiotensin system. In the mesenteric vascular bed, the elevated resistance in the arterial system is present in both the macroarteries and in the more distal microarteries and veins. Changes in resistance arteries include hypertrophy and reduction in outer diameter (remodelling). In the resistance arteries from human essential hypertensives, remodelling is the predominant finding. Long-term treatment with an angiotensin I converting enzyme inhibitor but not with a β-blocker was effective in reversing this type of vascular change. Studies have suggested that in addition to angiotensin II, endothelin may play a role in vascular remodelling of resistance arteries.Key words: hypertension, vascular, remodelling, smooth muscle, growth factors.

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48

Bowles, D. K., Q. Hu, M. H. Laughlin, and M. Sturek. "Heterogeneity of L-type calcium current density in coronary smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (October 1, 1997): H2083—H2089. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h2083.

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Heterogeneity of vascular responses to physiological and pharmacological stimuli has been demonstrated throughout the coronary circulation. Typically, this heterogeneity is based on vessel size. Although the cellular mechanisms for this heterogeneity are unknown, one plausible factor may be heterogeneous distribution of ion channels important in regulation of vascular tone. Because of the importance of voltage-gated Ca2+ channels in regulation of vascular tone, we hypothesized that these channels would be unequally distributed throughout the coronary arterial bed. To test this hypothesis, voltage-gated Ca2+current was measured in smooth muscle from conduit arteries (>1.0 mm), small arteries (200–250 μm), and large arterioles (75–125 μm) of miniature swine using whole cell voltage-clamp techniques. With 2 mM Ca2+ or 10 mM Ba2+ as charge carrier, voltage-gated Ca2+ current density was inversely related to arterial diameter, i.e., large arterioles > small arteries > conduit. Peak inward currents (10 mM Ba2+) were increased ∼2.5- and ∼1.5-fold in large arterioles and small arteries, respectively, compared with conduit arteries (−5.58 ± 0.53, −3.54 ± 0.34, and −2.26 ± 0.31 pA/pF, respectively). In physiological Ca2+ (2 mM), small arteries demonstrated increased inward current at membrane potentials within the physiological range for vascular smooth muscle (as negative as −40 mV) compared with conduit arteries. In addition, cells from large arterioles showed a negative shift in the membrane potential for half-maximal activation compared with small and conduit arteries (−13.23 ± 0.88, −6.22 ± 1.35, and −8.62 ± 0.81 mV, respectively; P < 0.05). Voltage characteristics and dihydropyridine sensitivity identified this Ca2+ current as predominantly L-type current in all arterial sizes. We conclude that L-type Ca2+ current density is inversely related to arterial diameter within the coronary arterial vasculature. This heterogeneity of Ca2+ current density may provide, in part, the basis for functional heterogeneity within the coronary circulation.

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Nelson, M. T., J. B. Patlak, J. F. Worley, and N. B. Standen. "Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone." American Journal of Physiology-Cell Physiology 259, no. 1 (July 1, 1990): C3—C18. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c3.

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Resistance arteries exist in a maintained contracted state from which they can dilate or constrict depending on need. In many cases, these arteries constrict to membrane depolarization and dilate to membrane hyperpolarization and Ca-channel blockers. We discuss recent information on the regulation of arterial smooth muscle voltage-dependent Ca channels by membrane potential and vasoconstrictors and on the regulation of membrane potential and K channels by vasodilators. We show that voltage-dependent Ca channels in the steady state can be open and very sensitive to membrane potential changes in a range that occurs in resistance arteries with tone. Many synthetic and endogenous vasodilators act, at least in part, through membrane hyperpolarization caused by opening K channels. We discuss evidence that these vasodilators act on a common target, the ATP-sensitive K (KATP) channel that is inhibited by sulfonylurea drugs. We propose the following hypotheses that presently explain these findings: 1) arterial smooth muscle tone is regulated by membrane potential primarily through the voltage dependence of Ca channels; 2) many vasoconstrictors act, in part, by opening voltage-dependent Ca channels through membrane depolarization and activation by second messengers; and 3) many vasodilators work, in part, through membrane hyperpolarization caused by KATP channel activation.

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Ray, Julie Basu, Sara Arab, Yupu Deng, Peter Liu, Linda Penn, David W. Courtman, and Michael E. Ward. "Oxygen regulation of arterial smooth muscle cell proliferation and survival." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H839—H852. http://dx.doi.org/10.1152/ajpheart.00587.2007.

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The purpose of this study was to determine if hypoxia elicits different proliferative and apoptotic responses in systemic arterial smooth muscle cells incubated under conditions that do or do not result in cellular ATP depletion and whether these effects are relevant to vascular remodeling in vivo. Gene expression profiling was used to identify potential regulatory pathways. In human aortic smooth muscle cells (HASMCs) incubated at 3% O2, proliferation and progression through the G1/S interphase are enhanced. Incubation at 1% O2 reduced proliferation, delayed G1/S transition, increased apoptotic cell death, and is associated with mitochondrial membrane depolarization and reduced cellular ATP levels. In aorta and mesenteric artery from rats exposed to hypoxia (10% O2, 48 h), both proliferation and apoptosis are increased, as are medial nuclear density and smooth muscle cell content. Although nuclear levels of hypoxia-inducible factor 1-α (HIF-1α) are increased to a similar extent in HASMCs incubated at 1 and 3% O2, expression of tumor protein p53, its transcriptional target p21, as well as their regulatory factors and downstream effectors, are differentially affected under these two conditions, suggesting that the bidirectional effects of hypoxia are mediated by this pathway. We conclude that hypoxia induces a state of enhanced cell turnover through increased rates of both smooth muscle cell proliferation and death. This confers the ability to remodel the vasculature in response to changing tissue metabolic needs while avoiding the accumulation of mutations that may lead to malignant transformation or the formation of abnormal vascular structures.

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Journal articles on the topic 'Arterial Smooth Muscle Cell'

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