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Phenotypic Switching Of Vascular Smooth Muscle Cells In Atherosclerosis Journal Of The American Heart Association

Sorry, a shareable link is not currently available for this article. Changes in the retardation of cells treated with contraction and relaxation chemicals against controls were evaluated at each time point using Steel’s test. At each time point, the cell area, ACell, was measured by manually outlining the shape of the VSMCs in the phase contrast images. Because the retardation in background areas changed with time, a background image was taken just before imaging a cell. Retardations of passage 2 and 12 cells were compared because lower passage VSMCs have a contractile phenotype, while higher passage VSMCs dedifferentiate towards the synthetic phenotype39. VSMCs with the contractile phenotype show a higher retardation than those with the synthetic phenotype, suggesting that retardation can be used to evaluate VSMC phenotype.

Cholesterol‐induced phenotypic modulation of smooth muscle cells to macrophage/fibroblast‐like cells is driven by an unfolded protein response. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage‐like state after cholesterol loading. Low LAL (lysosomal acid lipase) expression by smooth muscle cells relative to macrophages as a mechanism for arterial foam cell formation. Contribution of intimal smooth muscle cells to cholesterol accumulation and macrophage‐like cells in human atherosclerosis. BMAL1 modulates smooth muscle cells phenotypic switch towards fibroblast‐like cells and stabilizes atherosclerotic plaques by upregulating YAP1.

Intimal smooth muscle cells of porcine and human coronary artery express S100A4, a marker of the rhomboid phenotype in vitro. Single‐cell genomics reveals a novel cell state during smooth muscle cell phenotypic switching and potential therapeutic targets for atherosclerosis in mouse and human. Cao G, Xuan X, Hu J, Zhang R, Jin H, Dong H. How vascular smooth muscle cell phenotype switching contributes to vascular disease. ACTA indicates α‐smooth muscle actin; CArG, CC(A/T‐rich)6GG cis‐regulating element; Itga8, integrin alpha 8; Myh11, myosin heavy chain 11; SRF, serum response factor; Tagln, transgelin; and VSMC, vascular smooth muscle cell. Some potential markers include platelet‐derived growth factor receptor beta and S100A4.13, 21, 22 Of note, the contraction mechanism of myofibroblasts is different from that of VSMCs.52, 53 Thus, it is possible that analyzing the contractile characteristics can help distinguish myofibroblast‐like VSMCs from VSMCs. VSMCs phenotype switching provides a new perspective for understanding the pathogenesis of vascular diseases. Great progress has been made in the study of the role of VSMCs phenotype transformation in vascular diseases in the past 20 years.

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Shi J, Yang Y, Cheng A, Xu G, He F. Metabolism of vascular smooth muscle cells in vascular diseases. Atherosclerotic plaques are characterized by the accumulation of cholesterol crystals in the arterial wall, a fibrous cap rich in extracellular matrix produced by vascular smooth muscle cells (VSMCs) and infiltration of immune cells (such as monocytes-macrophages, T cells, and mast cells) 3, 4. Photoelasticity-based evaluation of cellular contractile force for phenotypic discrimination of vascular smooth muscle cells. Photoelasticity-based evaluation of cellular contractile force for phenotypic discrimination of vascular smooth oosch casino muscle cells Coronary artery bypass grafting, intimal hyperplasia, phenotypic switching, vascular smooth muscle cells, vein graft failure Zargham R, Touyz RM, Thibault G. Alpha 8 integrin overexpression in de‐differentiated vascular smooth muscle cells attenuates migratory activity and restores the characteristics of the differentiated phenotype. Generation and comparative analysis of an Itga8‐CreER (T2) mouse with preferential activity in vascular smooth muscle cells. Shioi A, Nishizawa Y, Jono S, Koyama H, Hosoi M, Morii H. Beta‐glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells.

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Adipocyte‐derived factors regulate vascular smooth muscle cells through mineralocorticoid and glucocorticoid receptors. Zhang F, Guo X, Xia Y, Mao L. An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis. Yoshida T, Yamashita M, Hayashi M. Kruppel‐like factor 4 contributes to high phosphate‐induced phenotypic switching of vascular smooth muscle cells into osteogenic cells. Nakahara T, Kawai‐Kowase K, Matsui H, Sunaga H, Utsugi T, Iso T, Arai M, Tomono S, Kurabayashi M. Fibroblast growth factor 23 inhibits osteoblastic gene expression and induces osteoprotegerin in vascular smooth muscle cells. Toll‐like receptor 4 mediated oxidized low‐density lipoprotein‐induced foam cell formation in vascular smooth muscle cells via Src and Sirt1/3 pathway. Burger F, Baptista D, Roth A, da Silva RF, Montecucco F, Mach F, Brandt KJ, Miteva K. NLRP3 inflammasome activation controls vascular smooth muscle cells phenotypic switch in atherosclerosis. Zhang Z, Huang J, Wang Y, Shen W. Transcriptome analysis revealed a two‐step transformation of vascular smooth muscle cells to macrophage‐like cells.

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For the very first time, agent of the Special Operations Executive (SOE), Harry Hawker steps out of the shadows as the lead protagonist While Sniper Elite 5 included updates set in Vichy France, the team decided to make a standalone game set in this location because the team "felt that there was much more to explore". The game retained the same gameplay systems, though the team added some new features, such as a new grenade type and a new timed-based mode. Once in Amiens, Hawker finds out that when he finishes his mission by trapping the Zugwerfers for an RAF bombing, he will not be able to escape in time. The dam from the first mission is being repaired, however, one of the crashed RAF bombers had a bouncing bomb, which the Germans are studying.

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Changes in retardation with time when the chemical reagent was applied to the cell to alter the cellular contraction state. Under the assumption that the refractive index stays constant, retardation measurements provide information on the mechanical state. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

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