To explore the key extracellular matrix (ECM) proteins in the maintenance of the contractile phenotype of vascular smooth muscle cells (VSMCs), investigators applied protein-protein interaction network analysis to explore novel ECM proteins associated with the VSMC phenotype.
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Mao, C., Ma, Z., Jia, Y., Li, W., Xie, N., Zhao, G., Ma, B., Yu, F., Sun, J., Zhou, Y., Cui, Q., Fu, Y., & Kong, W. (n.d.). Nidogen-2 Maintains the Contractile Phenotype of Vascular Smooth Muscle Cells and Prevents Neointima Formation via Bridging Jagged1-Notch3 Signaling. Circulation, 0(0). https://doi.org/10.1161/CIRCULATIONAHA.120.053361 Cite
Scientists revealed that MK2206 suppressed migration, proliferation, and inflammation in vascular smooth muscle cells. Moreover, MK2206 inhibited proliferation and inflammation of endothelial cells.
[Acta Pharmacologica Sinica]
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Scientists summarize the current understanding of exosome biogenesis and uptake, and discuss atherogenic and atheroprotective functions of exosomes secreted from these cell types.
The authors summarize the biogenesis, characteristics and functions of circRNAs with a focus on their roles in the pathogenesis of atherosclerosis.
Fluorescently labeled NLRP3 inflammasome particles were isolated from a mutant NLRP3-YFP cell line and used to treat primary human coronary artery smooth muscle cells for 4 and 24 hours.
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Scientists identified a vascular smooth muscle cell (VSMC)-enriched long noncoding RNA cardiac mesoderm enhancer-associated noncoding RNA (CARMN) that was dynamically regulated with progression of atherosclerosis. In both mouse and human atherosclerotic plaques, CARMN colocalized with VSMCs and was expressed in the nucleus.
[Arteriosclerosis Thrombosis and Vascular Biology]
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Researchers used loss/gain-of-function approaches by gene delivery to determine whether cytokine induced apoptosis inhibitor 1 (CIAPIN1) modulated vascular smooth muscle cell proliferation, migration, and neointima formation, and to define the underlying mechanisms.
[British Journal of Pharmacology]
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Researchers found that erythropoietin (EPO) promoted the formation of abdominal aortic aneurysm (AAA) in both Apoe−/− and wild type mice by enhancing angiogenesis, inflammation, collagen degradation, and apoptosis of smooth muscle cells and that EPO/EPO receptor signaling was essential for angiotensin II-induced AAA.
[Science Translational Medicine]
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Investigators used isolated murine mesentery arterioles and co-cultures of human coronary artery endothelial cells and smooth muscle cells to test the hypothesis that heme oxygenase 1 mediated the effects of fluid shear stress on placental growth factor.
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Researchers investigated the effects of nicotine on initiation of vascular smooth muscle cell (VSMC) calcification. In vitro, nicotine induced human primary VSMC calcification, increased osteogenic gene expression, and extracellular vesicle secretion.
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The authors examined the role of Sirtuin1 (Sirt1) in Angiotensin II (Ang II)-induced overexpression of Giα proteins and hyperproliferation of aortic vascular smooth muscle cells (VSMCs). Ang II treatment of VSMCs increased the expression of Sirt1 which was attenuated by AT1 and AT2 receptor antagonists, losartan and PD123319 respectively.
[American Journal of Physiology-Heart and Circulatory Physiology]
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