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Your search keyword '"Cosentino, S"' showing total 21 results
Start Over Author "Cosentino, S" Publisher elsevier bv
21 results on '"Cosentino, S"'

3. A PET-based radiomics model of brain metastasis

Author

Stefano, A., primary, Comelli, A., additional, Barone, S., additional, Savoca, G., additional, Richiusa, S., additional, Sabini, M.G., additional, Cosentino, S., additional, Ippolito, M., additional, and Russo, G., additional

Published
2021
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21. Statins prevent tissue factor induction by protease-activated receptors 1 and 2 in human umbilical vein endothelial cells in vitro

Author

Angela Pirillo, Simona Cosentino, Luciana Mussoni, Cristina Banfi, Sabrina Lento, Elena Tremoli, Maura Brioschi, Stefano Galli, Banfi, C, Brioschi, M, Lento, S, Pirillo, A, Galli, S, Cosentino, S, Tremoli, E, and Mussoni, L

Subjects
Indoles, Caveolin 1, Umbilical vein, Fatty Acids, Monounsaturated, Membrane microdomain, Endothelial cell, Protease-activated receptor, Phosphorylation, Rosuvastatin Calcium, Receptor, Cells, Cultured, Mitogen-Activated Protein Kinase 1, Sulfonamides, Mitogen-Activated Protein Kinase 3, Hematology, GTP-Binding Protein alpha Subunits, Cell biology, Up-Regulation, Protein Transport, Cholesterol, src-Family Kinases, Biochemistry, cardiovascular system, Signal transduction, Proto-oncogene tyrosine-protein kinase Src, Signal Transduction, Cell signaling, Statin, medicine.drug_class, Mevalonic Acid, Biology, Thromboplastin, Tissue factor, Membrane Microdomains, medicine, Human Umbilical Vein Endothelial Cells, Humans, Receptor, PAR-2, Receptor, PAR-1, RNA, Messenger, Fluvastatin, Terpenes, Signaling, Enzyme Activation, Fluorobenzenes, Pyrimidines, Hydroxymethylglutaryl-CoA Reductase Inhibitors
Abstract

To cite this article: Banfi C, Brioschi M, Lento S, Pirillo A, Galli S, Cosentino S, Tremoli E, Mussoni L. Statins prevent tissue factor induction by protease-activated receptors 1 and 2 in human umbilical vein endothelial cells in vitro. J Thromb Haemost 2011; 9: 1608–19. Summary. Background: Protease-activated receptors (PARs) are G-protein-coupled receptors that function in hemostasis and thrombosis, as well as in the inflammatory and proliferative responses triggered by tissue injury. We have previously shown that PAR1 or PAR2 occupancy by specific PAR-agonist peptides (PAR-APs) induces tissue factor (TF) expression in human umbilical vein endothelial cells (HUVECs), where TF regulation by PAR1 (but not by PAR2) requires intact endothelial caveolin-enriched membrane microdomains in which PAR1 and caveolin-1 associate. Objectives: The aim of this study was to determine the effects of cholesterol-lowering agents (statins) and cholesterol-loading lipoprotein on PAR1-AP-mediated and PAR2-AP-mediated TF induction in HUVECs. Results: Statins completely prevented TF induction by PAR-APs in an isoprenoid-independent manner, induced the delocalization of PAR1 from caveolin-enriched membrane microdomains without affecting PAR1 mRNA, and decreased PAR2 mRNA and protein levels. Statins also prevented PAR-AP-mediated extracellular signal-related kinase 1/2 activation, which is crucial for TF induction. The redistribution of PAR1 is accompanied by the relocation of the membrane microdomain-associated G-protein α, caveolin-1, and Src, which we previously showed to play a key role in signal transduction and TF induction. Conversely, cholesterol loading potently amplified PAR1-AP-induced TF, probably as a result of the increased abundance of PAR1 and the Src and G-protein α signaling molecules in the caveolin-1-enriched fraction, without affecting PAR1 mRNA. Conclusions: As PARs have important functions in hemostasis, cancer, thrombosis, and inflammatory processes, our findings that statins prevent TF induction by PAR-APs altering the membrane localization of PAR1 and the expression of PAR2 suggest that they may provide health benefits other than reducing atherosclerosis.

Published
2011

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