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Your search keyword '"Crucet, Margot"' showing total 11 results
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11 results on '"Crucet, Margot"'

1. Inhibition of de novo ceramide synthesis by Sirtuin-1 improves beta-cell function and glucose metabolism in type 2 diabetes

Author

Velagapudi, Srividya, primary, Karsai, Gergely, additional, Karsai, Maria, additional, Mohammed, Shafeeq A, additional, Montecucco, Fabrizio, additional, Liberale, Luca, additional, Lee, Hwan, additional, Carbone, Federico, additional, Francesco Adami, Giovanni, additional, Yang, Kangmin, additional, Crucet, Margot, additional, Stein, Sokrates, additional, Paneni, Franceso, additional, Lapikova-Bryhinska, Tetiana, additional, Jang, Hyun-Duk, additional, Kraler, Simon, additional, Vdovenko, Daria, additional, Arnold Züllig, Richard, additional, Camici, Giovanni G, additional, Kim, Hyo-Soo, additional, Laaksonen, Reijo, additional, Gerber, Philipp A, additional, Hornemann, Thorsten, additional, Akhmedov, Alexander, additional, and Lüscher, Thomas F, additional

Published
2024
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5. TNFα induces endothelial dysfunction in rheumatoid arthritis via LOX-1 and arginase 2: reversal by monoclonal TNFα antibodies

Author

Akhmedov, Alexander, primary, Crucet, Margot, additional, Simic, Branko, additional, Kraler, Simon, additional, Bonetti, Nicole R, additional, Ospelt, Caroline, additional, Distler, Oliver, additional, Ciurea, Adrian, additional, Liberale, Luca, additional, Jauhiainen, Matti, additional, Metso, Jari, additional, Miranda, Melroy, additional, Cydecian, Rose, additional, Schwarz, Lena, additional, Fehr, Vera, additional, Zilinyi, Rita, additional, Amrollahi-Sharifabadi, Mohammad, additional, Ntari, Lydia, additional, Karagianni, Niki, additional, Ruschitzka, Frank, additional, Laaksonen, Reijo, additional, Vanhoutte, Paul M, additional, Kollias, George, additional, Camici, Giovanni G, additional, and Lüscher, Thomas F, additional

Published
2021
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6. TNFα induces endothelial dysfunction in rheumatoid arthritis via LOX-1 and arginase 2: reversal by monoclonal TNFα antibodies.

Author

Akhmedov, Alexander, Crucet, Margot, Simic, Branko, Kraler, Simon, Bonetti, Nicole R, Ospelt, Caroline, Distler, Oliver, Ciurea, Adrian, Liberale, Luca, Jauhiainen, Matti, Metso, Jari, Miranda, Melroy, Cydecian, Rose, Schwarz, Lena, Fehr, Vera, Zilinyi, Rita, Amrollahi-Sharifabadi, Mohammad, Ntari, Lydia, Karagianni, Niki, and Ruschitzka, Frank

Subjects
*ENDOTHELIUM diseases, *RHEUMATOID arthritis, *MONOCLONAL antibodies, *LDL cholesterol, *ARGINASE, *CARDIOLOGICAL manifestations of general diseases
Abstract

Aims Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting joints and blood vessels. Despite low levels of low-density lipoprotein cholesterol (LDL-C), RA patients exhibit endothelial dysfunction and are at increased risk of death from cardiovascular complications, but the molecular mechanism of action is unknown. We aimed in the present study to identify the molecular mechanism of endothelial dysfunction in a mouse model of RA and in patients with RA. Methods and results Endothelium-dependent relaxations to acetylcholine were reduced in aortae of two tumour necrosis factor alpha (TNFα) transgenic mouse lines with either mild (Tg3647) or severe (Tg197) forms of RA in a time- and severity-dependent fashion as assessed by organ chamber myograph. In Tg197 , TNFα plasma levels were associated with severe endothelial dysfunction. LOX-1 receptor was markedly up-regulated leading to increased vascular oxLDL uptake and NFκB-mediated enhanced Arg2 expression via direct binding to its promoter resulting in reduced NO bioavailability and vascular cGMP levels as shown by ELISA and chromatin immunoprecipitation. Anti-TNFα treatment with infliximab normalized endothelial function together with LOX-1 and Arg2 serum levels in mice. In RA patients, soluble LOX-1 serum levels were also markedly increased and closely related to serum levels of C-reactive protein. Similarly, ARG2 serum levels were increased. Similarly, anti-TNFα treatment restored LOX-1 and ARG2 serum levels in RA patients. Conclusions Increased TNFα levels not only contribute to RA, but also to endothelial dysfunction by increasing vascular oxLDL content and activation of the LOX-1/NFκB/Arg2 pathway leading to reduced NO bioavailability and decreased cGMP levels. Anti-TNFα treatment improved both articular symptoms and endothelial function by reducing LOX-1, vascular oxLDL, and Arg2 levels. [ABSTRACT FROM AUTHOR]

Published
2022
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7. Expression and regulation of 12/15-lipoxygenases in human primary macrophages

Author

Wuest, Sophia J A, Crucet, Margot, Gemperle, Claudio, Loretz, Christa, Hersberger, Martin, University of Zurich, and Hersberger, Martin

Subjects
10036 Medical Clinic, 10076 Center for Integrative Human Physiology, 570 Life sciences, biology, 610 Medicine & health, 2705 Cardiology and Cardiovascular Medicine
Published
2012

8. Politics

Author

Crucet, Margot and Velasco Montante, Astrid

Subjects
HUMANIDADES Y CIENCIAS DE LA CONDUCTA, Latin America, arte, América Latina, México, Ernesto Ríos, Mexico, fotografía
Published
2003

11. Expression of the G Protein-Coupled Receptor 68 is Increased by TNF-Mediated Inflammatory Signalling

Author

de Valliere, Cheryl, primary, Hiller, Christian, additional, Kellermeier, Silvia, additional, Crucet, Margot, additional, Vetter, Irina, additional, Inserra, Marco, additional, Lewis, Richard J., additional, Cooper, Matthew A., additional, Vidal, Solange, additional, Seuwen, Klaus, additional, Wagner, Carsten A., additional, Fried, Michael, additional, Kullak-Ublick, Gerd A., additional, Rogler, Gerhard, additional, and Eloranta, Jyrki J., additional

Published
2011
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