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211 results on '"Paulsson-Berne, Gabrielle"'

4. Novel Multiomics Profiling of Human Carotid Atherosclerotic Plaques and Plasma Reveals Biliverdin Reductase B as a Marker of Intraplaque Hemorrhage

Author

Matic, Ljubica Perisic, Jesus Iglesias, Maria, Vesterlund, Mattias, Lengquist, Mariette, Hong, Mun-Gwan, Saieed, Shanga, Sanchez-Rivera, Laura, Berg, Martin, Razuvaev, Anton, Kronqvist, Malin, Lund, Kent, Caidahl, Kenneth, Gillgren, Peter, Pontén, Fredrik, Uhlén, Mathias, Schwenk, Jochen M., Hansson, Göran K., Paulsson-Berne, Gabrielle, Fagman, Erika, Roy, Joy, Hultgren, Rebecka, Bergström, Göran, Lehtiö, Janne, Odeberg, Jacob, and Hedin, Ulf

Published
2018
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6. The resolvin D1 receptor GPR32 transduces inflammation resolution and atheroprotection

Author

Arnardottir, Hildur, Thul, Silke, Pawelzik, Sven-Christian, Karadimou, Glykeria, Artiach, Gonzalo, Gallina, Alessandro L., Mysdotter, Victoria, Carracedo, Miguel, Tarnawski, Laura, Caravaca, April S., Baumgartner, Roland, Ketelhuth, Daniel F.J., Olofsson, Peder S., Paulsson-Berne, Gabrielle, Hansson, Goran K., and Back, Magnus

Subjects
Cell receptors -- Health aspects, Atherosclerosis -- Development and progression -- Care and treatment -- Genetic aspects, Health care industry
Abstract

Chronic inflammation is a hallmark of atherosclerosis and results from an imbalance between proinflammatory and proresolving signaling. The human GPR32 receptor, together with the ALX/FPR2 receptor, transduces biological actions of several proresolving mediators that stimulate resolution of inflammation. However, since no murine homologs of the human GPR32 receptor exist, comprehensive in vivo studies are lacking. Using human atherosclerotic lesions from carotid endarterectomies and creating a transgenic mouse model expressing human GPR32 on a Fpr2xApoE doubleKO background ([hGPR32.sub.myc] * [Fpr.sup.2-/-] * [Apoe.sup.-/-]), we investigated the role of GPR32 in atherosclerosis and self-limiting acute inflammation. GPR32 mRNA was reduced in human atherosclerotic lesions and correlated with the immune cell markers ARG1, NOS2, and FOXP3. Atherosclerotic lesions, necrotic core, and aortic inflammation were reduced in [hGPR32.sub.myc]Tg * [Fpr2.sup.-/-] * [Apoe.sup.-/-] transgenic mice as compared with [Fpr2.sup.-/-] * [Apoe.sup.-/-] nontransgenic littermates. In a zymosan-induced peritonitis model, the [hGPR32.sub.myc]Tg * [Fpr2.sub.-/-] * [Apoe.sub.-/-] transgenic mice had reduced inflammation at 4 hours and enhanced proresolving macrophage responses at 24 hours compared with nontransgenic littermates. The GPR32 agonist aspirin-triggered resolvin D1 (AT-RvD1) regulated leukocyte responses, including enhancing macrophage phagocytosis and intracellular signaling in [hGPR32.sub.myc]Tg * [Fpr2.sup.-/-] * [Apoe.sup.-/-] transgenic mice, but not in [Fpr2.sup.-/-] * [Apoe.sup.-/-] nontransgenic littermates. Together, these results provide evidence that GPR32 regulates resolution of inflammation and is atheroprotective in vivo., Introduction Resolution of acute inflammation is an active, coordinated response aimed at terminating the inflammatory response and restoring tissue homeostasis (1). Resolution of inflammation is regulated by a superfamily of [...]

Published
2021
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7. PCSK6 Is a Key Protease in the Control of Smooth Muscle Cell Function in Vascular Remodeling

Author

Rykaczewska, Urszula, Suur, Bianca E., Röhl, Samuel, Razuvaev, Anton, Lengquist, Mariette, Sabater-Lleal, Maria, van der Laan, Sander W., Miller, Clint L., Wirka, Robert C., Kronqvist, Malin, Gonzalez Diez, Maria, Vesterlund, Mattias, Gillgren, Peter, Odeberg, Jacob, Lindeman, Jan H., Veglia, Fabrizio, Humphries, Steve E., de Faire, Ulf, Baldassarre, Damiano, Tremoli, Elena, Lehtiö, Janne, Hansson, Göran K., Paulsson-Berne, Gabrielle, Pasterkamp, Gerard, Quertermous, Thomas, Hamsten, Anders, Eriksson, Per, Hedin, Ulf, and Matic, Ljubica

Published
2020
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9. ERV1/ChemR23 Signaling Protects Against Atherosclerosis by Modifying Oxidized Low-Density Lipoprotein Uptake and Phagocytosis in Macrophages

Author

Laguna-Fernandez, Andres, Checa, Antonio, Carracedo, Miguel, Artiach, Gonzalo, Petri, Marcelo H., Baumgartner, Roland, Forteza, Maria J., Jiang, Xintong, Andonova, Teodora, Walker, Mary E., Dalli, Jesmond, Arnardottir, Hildur, Gisterå, Anton, Thul, Silke, Wheelock, Craig E., Paulsson-Berne, Gabrielle, Ketelhuth, Daniel F.J., Hansson, Göran K., and Bäck, Magnus

Published
2018
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10. MicroRNA-210 Enhances Fibrous Cap Stability in Advanced Atherosclerotic Lesions

Author

Eken, Suzanne M., Jin, Hong, Chernogubova, Ekaterina, Li, Yuhuang, Simon, Nancy, Sun, Changyan, Korzunowicz, Greg, Busch, Albert, Bäcklund, Alexandra, Österholm, Cecilia, Razuvaev, Anton, Renné, Thomas, Eckstein, Hans Henning, Pelisek, Jaroslav, Eriksson, Per, González Díez, María, Perisic Matic, Ljubica, Schellinger, Isabel N., Raaz, Uwe, Leeper, Nicholas J., Hansson, Göran K., Paulsson-Berne, Gabrielle, Hedin, Ulf, and Maegdefessel, Lars

Published
2017
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14. AMPA-Type Glutamate Receptors Associated With Vascular Smooth Muscle Cell Subpopulations in Atherosclerosis and Vascular Injury

Author

Gallina, Alessandro L., Rykaczewska, Urszula, Wirka, Robert C., Caravaca, April S., Shavva, Vladimir S., Youness, Mohamad, Karadimou, Glykeria, Lengquist, Mariette, Razuvaev, Anton, Paulsson-Berne, Gabrielle, Quertermous, Thomas, Gisterå, Anton, Malin, Stephen G., Tarnawski, Laura, Matic, Ljubica, and Olofsson, Peder S.

Subjects
VAGUS NERVE-STIMULATION, Science & Technology, Cardiac & Cardiovascular Systems, ENDARTERECTOMY, glutamate, Cardiovascular Medicine, R/BIOCONDUCTOR PACKAGE, DISEASE, smooth muscle cells, neuroscience, GluA2, inflammation, cardiovascular system, Cardiovascular System & Cardiology, atherosclerosis, Life Sciences & Biomedicine, INTEGRATION, GluA1, Original Research, neurotransmitter, GENE-EXPRESSION
Abstract

Objectives and Aims: Vascular smooth muscle cells (VSMCs) are key constituents of both normal arteries and atherosclerotic plaques. They have an ability to adapt to changes in the local environment by undergoing phenotypic modulation. An improved understanding of the mechanisms that regulate VSMC phenotypic changes may provide insights that suggest new therapeutic targets in treatment of cardiovascular disease (CVD). The amino-acid glutamate has been associated with CVD risk and VSMCs metabolism in experimental models, and glutamate receptors regulate VSMC biology and promote pulmonary vascular remodeling. However, glutamate-signaling in human atherosclerosis has not been explored. Methods and Results: We identified glutamate receptors and glutamate metabolism-related enzymes in VSMCs from human atherosclerotic lesions, as determined by single cell RNA sequencing and microarray analysis. Expression of the receptor subunits glutamate receptor, ionotropic, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA)-type subunit 1 (GRIA1) and 2 (GRIA2) was restricted to cells of mesenchymal origin, primarily VSMCs, as confirmed by immunostaining. In a rat model of arterial injury and repair, changes of GRIA1 and GRIA2 mRNA level were most pronounced at time points associated with VSMC proliferation, migration, and phenotypic modulation. In vitro, human carotid artery SMCs expressed GRIA1, and selective AMPA-type receptor blocking inhibited expression of typical contractile markers and promoted pathways associated with VSMC phenotypic modulation. In our biobank of human carotid endarterectomies, low expression of AMPA-type receptor subunits was associated with higher content of inflammatory cells and a higher frequency of adverse clinical events such as stroke. Conclusion: AMPA-type glutamate receptors are expressed in VSMCs and are associated with phenotypic modulation. Patients suffering from adverse clinical events showed significantly lower mRNA level of GRIA1 and GRIA2 in their atherosclerotic lesions compared to asymptomatic patients. These results warrant further mapping of neurotransmitter signaling in the pathogenesis of human atherosclerosis. ispartof: FRONTIERS IN CARDIOVASCULAR MEDICINE vol:8 ispartof: location:Switzerland status: published

Published
2021

15. BS25 TAM receptor AXL loss regulates smooth muscle cell differentiation and accelerates atherosclerosis in mice

Author

Mcshane, Lucy, primary, Gurgone, Danila, additional, Bin-Khunayn, Abdullatif Mohammed, additional, Crespo, Eva, additional, Grassia, Gianluca, additional, MacRitchie, Neil, additional, Giacca, Mauro, additional, Zentilin, Lorena, additional, Karadimou, Glykeria, additional, Paulsson-Berne, Gabrielle, additional, Olofsson, Peder S, additional, Otto, Thomas D, additional, Guzik, Tomasz J, additional, Kurowska-Stolarska, Mariola, additional, and Maffia, Pasquale, additional

Published
2021
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18. AMPA-Type Glutamate Receptors Associated With Vascular Smooth Muscle Cell Subpopulations in Atherosclerosis and Vascular Injury

Author

Gallina, Alessandro L., primary, Rykaczewska, Urszula, additional, Wirka, Robert C., additional, Caravaca, April S., additional, Shavva, Vladimir S., additional, Youness, Mohamad, additional, Karadimou, Glykeria, additional, Lengquist, Mariette, additional, Razuvaev, Anton, additional, Paulsson-Berne, Gabrielle, additional, Quertermous, Thomas, additional, Gisterå, Anton, additional, Malin, Stephen G., additional, Tarnawski, Laura, additional, Matic, Ljubica, additional, and Olofsson, Peder S., additional

Published
2021
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19. sj-docx-1-vmj-10.1177_1358863X20977662 – Supplemental material for Expression of Interleukin 6 signaling receptors in carotid atherosclerosis

Author

Ziegler, Louise, Lundqvist, Jasmin, Dreij, Kristian, Wallén, Håkan, Faire, Ulf De, Paulsson-Berne, Gabrielle, Hedin, Ulf, Matic, Ljubica, and Gigante, Bruna

Subjects
FOS: Clinical medicine, Cardiology, 110323 Surgery
Abstract

Supplemental material, sj-docx-1-vmj-10.1177_1358863X20977662 for Expression of Interleukin 6 signaling receptors in carotid atherosclerosis by Louise Ziegler, Jasmin Lundqvist, Kristian Dreij, Håkan Wallén, Ulf de Faire, Gabrielle Paulsson-Berne, Ulf Hedin, Ljubica Matic and Bruna Gigante in Vascular Medicine

Published
2020
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20. Expression of CARD8 in human atherosclerosis and its regulation of inflammatory proteins in human endothelial cells

Author

Paramel Varghese, Geena, Karadimou, Glykeria, Göthlin Eremo, Anna, Ljungberg, Liza, Hedin, Ulf, Olofsson, Peder S., Folkersen, Lasse, Paulsson Berne, Gabrielle, Sirsjö, Allan, Fransén, Karin, Paramel Varghese, Geena, Karadimou, Glykeria, Göthlin Eremo, Anna, Ljungberg, Liza, Hedin, Ulf, Olofsson, Peder S., Folkersen, Lasse, Paulsson Berne, Gabrielle, Sirsjö, Allan, and Fransén, Karin

Abstract

The Caspase activation and recruitment domain 8 (CARD8) protein is a component of innate immunity and overexpression of CARD8 mRNA was previously identified in atherosclerosis. However, very little is known about the regulation of CARD8 in endothelial cells and atherosclerosis. The aim of this study was to investigate CARD8 in the regulation of cytokine and chemokine expression in endothelial cells. Sections of human atherosclerotic lesions and non-atherosclerotic arteries were immunostained for CARD8 protein. Expression of CARD8 was correlated to mediators of inflammation in atherosclerotic lesions using Biobank of Karolinska Endarterectomies microarray data. The CARD8 mRNA was knocked-down in human umbilical vein endothelial cells (HUVECs) in vitro, followed by quantitative RT-PCR analysis and OLINK Proteomics. Endothelial and smooth muscle cells in arterial tissue expressed CARD8 and CARD8 correlated with vWF, CD163 and the expression of inflammatory genes, such as CXCL1, CXCL6 and PDGF-A in plaque. Knock-down of CARD8 in HUVECs significantly altered proteins involved in inflammatory response, such as CXCL1, CXCL6, PDGF-A, MCP-1 and IL-6. The present study suggest that CARD8 regulate the expression of cytokines and chemokines in endothelial cells and atherosclerotic lesions, suggesting that CARD8 plays a significant role in endothelial activation., An Author Correction to this article was published in Sci Rep. 2021 Apr 19;11(1):8852. doi: 10.1038/s41598-021-88467-2.

Published
2020
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21. PCSK6 Is a Key Protease in the Control of Smooth Muscle Cell Function in Vascular Remodeling

Author

CDL Onderzoek Pasterkamp, dLAB Afdelingen, Circulatory Health, Rykaczewska, Urszula, Suur, Bianca E, Röhl, Samuel, Razuvaev, Anton, Lengquist, Mariette, Sabater-Lleal, Maria, van der Laan, Sander W, Miller, Clint L, Wirka, Robert C, Kronqvist, Malin, Gonzalez Diez, Maria, Vesterlund, Mattias, Gillgren, Peter, Odeberg, Jacob, Lindeman, Jan Hn, Veglia, Fabrizio, Humphries, Steve E, de Faire, Ulf, Baldassarre, Damiano, Tremoli, Elena, Lehtiö, Janne, Hansson, Göran K, Paulsson-Berne, Gabrielle, Pasterkamp, Gerard, Quertermous, Thomas, Hamsten, Anders, Eriksson, Per, Hedin, Ulf, Matic, Ljubica, CDL Onderzoek Pasterkamp, dLAB Afdelingen, Circulatory Health, Rykaczewska, Urszula, Suur, Bianca E, Röhl, Samuel, Razuvaev, Anton, Lengquist, Mariette, Sabater-Lleal, Maria, van der Laan, Sander W, Miller, Clint L, Wirka, Robert C, Kronqvist, Malin, Gonzalez Diez, Maria, Vesterlund, Mattias, Gillgren, Peter, Odeberg, Jacob, Lindeman, Jan Hn, Veglia, Fabrizio, Humphries, Steve E, de Faire, Ulf, Baldassarre, Damiano, Tremoli, Elena, Lehtiö, Janne, Hansson, Göran K, Paulsson-Berne, Gabrielle, Pasterkamp, Gerard, Quertermous, Thomas, Hamsten, Anders, Eriksson, Per, Hedin, Ulf, and Matic, Ljubica

Published
2020

27. Genetic susceptibility loci for cardiovascular disease and their impact on atherosclerotic plaques

Author

van der Laan, Sander W., Siemelink, Marten A., Haitjema, Saskia, Foroughi Asl, Hassan, Perisic, Ljubica, Mokry, Michal, van Setten, Jessica, Malik, Rainer, Dichgans, Martin, Worrall, Bradford B, Samani, Nilesh J, Schunkert, Heribert, Erdmann, Jeanette, Hedin, Ulf, Paulsson-Berne, Gabrielle, Björkegrenn, Johan L.M, de Borst, Gert J., Asselbergs, Folkert W, den Ruijter, Folkert W, de Bakker, Paul I.W, Pasterkamp, Gerard, Ford, Ian, Sattar, Naveed, and Stott, David J.

Subjects
R1
Abstract

Background:\ud Atherosclerosis is a chronic inflammatory disease in part caused by lipid uptake in the vascular wall, but the exact underlying mechanisms leading to acute myocardial infarction and stroke remain poorly understood. Large consortia identified genetic susceptibility loci that associate with large artery ischemic stroke and coronary artery disease. However, deciphering their underlying mechanisms are challenging. Histological studies identified destabilizing characteristics in human atherosclerotic plaques that associate with clinical outcome. To what extent established susceptibility loci for large artery ischemic stroke and coronary artery disease relate to plaque characteristics is thus far unknown but may point to novel mechanisms.\ud \ud Methods:\ud We studied the associations of 61 established cardiovascular risk loci with 7 histological plaque characteristics assessed in 1443 carotid plaque specimens from the Athero-Express Biobank Study. We also assessed if the genotyped cardiovascular risk loci impact the tissue-specific gene expression in 2 independent biobanks, Biobank of Karolinska Endarterectomy and Stockholm Atherosclerosis Gene Expression.\ud \ud Results:\ud A total of 21 established risk variants (out of 61) nominally associated to a plaque characteristic. One variant (rs12539895, risk allele A) at 7q22 associated to a reduction of intraplaque fat, P=5.09×10−6 after correction for multiple testing. We further characterized this 7q22 Locus and show tissue-specific effects of rs12539895 on HBP1 expression in plaques and COG5 expression in whole blood and provide data from public resources showing an association with decreased LDL (low-density lipoprotein) and increase HDL (high-density lipoprotein) in the blood.\ud \ud Conclusions:\ud Our study supports the view that cardiovascular susceptibility loci may exert their effect by influencing the atherosclerotic plaque characteristics.

Published
2018

28. Prevention of radiotherapy-induced arterial inflammation by interleukin-1 blockade

Author

Christersdottir, Tinna, primary, Pirault, John, additional, Gisterå, Anton, additional, Bergman, Otto, additional, Gallina, Alessandro L, additional, Baumgartner, Roland, additional, Lundberg, Anna M, additional, Eriksson, Per, additional, Yan, Zhong-Qun, additional, Paulsson-Berne, Gabrielle, additional, Hansson, Göran K, additional, Olofsson, Peder S, additional, and Halle, Martin, additional

Published
2019
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29. Deficiency of the T cell regulator Casitas B-cell lymphoma-B aggravates atherosclerosis by inducing CD8+ T cell-mediated macrophage death

Author

Seijkens, Tom T P, primary, Poels, Kikkie, additional, Meiler, Svenja, additional, van Tiel, Claudia M, additional, Kusters, Pascal J H, additional, Reiche, Myrthe, additional, Atzler, Dorothee, additional, Winkels, Holger, additional, Tjwa, Marc, additional, Poelman, Hessel, additional, Slütter, Bram, additional, Kuiper, Johan, additional, Gijbels, Marion, additional, Kuivenhoven, Jan Albert, additional, Matic, Ljubica Perisic, additional, Paulsson-Berne, Gabrielle, additional, Hedin, Ulf, additional, Hansson, Göran K, additional, Nicolaes, Gerry A F, additional, Daemen, Mat J A P, additional, Weber, Christian, additional, Gerdes, Norbert, additional, de Winther, Menno P J, additional, and Lutgens, Esther, additional

Published
2018
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30. Endogenous control genes in complex vascular tissue samples

Author

Gabrielsen Anders, Agardh Hanna E, Razuvaev Anton, Kurtovic Sanela, Folkersen Lasse, and Paulsson-Berne Gabrielle

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background Gene expression microarrays and real-time PCR are common methods used to measure mRNA levels. Each method has a fundamentally different approach of normalization between samples. Relative quantification of gene expression using real-time PCR is often done using the 2^(-ΔΔCt) method, in which the normalization is performed using one or more endogenous control genes. The choice of endogenous control gene is often arbitrary or bound by tradition. We here present an analysis of the differences in expression results obtained with microarray and real-time PCR, dependent on different choices of endogenous control genes. Results In complex tissue, microarray data and real-time PCR data show the best correlation when endogenous control genes are omitted and the normalization is done relative to total RNA mass, as measured before reverse transcription. Conclusion We have found that for real-time PCR in heterogeneous tissue samples, it may be a better choice to normalize real-time PCR Ct values to the carefully measured mass of total RNA than to use endogenous control genes. We base this conclusion on the fact that total RNA mass normalization of real-time PCR data shows better correlation to microarray data. Because microarray data use a different normalization approach based on a larger part of the transcriptome, we conclude that omitting endogenous control genes will give measurements more in accordance with actual concentrations.

Published
2009
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31. Expression of Interleukin 6 signaling receptors in carotid atherosclerosis.

Author

Ziegler, Louise, Lundqvist, Jasmin, Dreij, Kristian, Wallén, Håkan, de Faire, Ulf, Paulsson-Berne, Gabrielle, Hedin, Ulf, Matic, Ljubica, and Gigante, Bruna

Subjects
ATHEROSCLEROSIS, ATHEROSCLEROTIC plaque, INTERLEUKIN-6, CAROTID artery, CAROTID artery diseases
Abstract

Interleukin (IL) 6 contributes to atherosclerotic plaque development through IL6 membrane-bound (IL6R and gp130) and soluble (sIL6R and sgp130) receptors. We investigated IL6 receptor expression in carotid plaques and its correlation with circulating IL6 and soluble receptor levels. Plasma samples and carotid plaques were obtained from 78 patients in the Biobank of Karolinska Endarterectomies study. IL6, sIL6R, and sgp130 were measured in plasma and IL6, IL6R, sIL6R, GP130, and s GP130-RAPS (s GP130) gene expression assessed in carotid plaques. Correlations between plaque IL6 signaling gene expression and plasma levels were determined by Spearman's correlation. Differences in plasma and gene expression levels between patients with (n = 53) and without (n = 25) a history of a cerebral event and statin-treated (n = 65) and non-treated (n = 11), were estimated by Kruskal–Wallis. IL6 and its receptors were all expressed in carotid plaques. There was a positive, borderline significant, moderate correlation between plasma IL6 and sIL6R and the respective gene expression levels (rho 0.23 and 0.22, both p = 0.05). IL6R expression was higher in patients with a history of a cerebrovascular event compared to those without (p = 0.007). Statin-treated had higher IL6R, sIL6R, and s GP130 expression levels and plasma sIL6R compared to non-treated patients (all p < 0.05). In conclusion, all components of the IL6 signaling pathways are expressed in carotid artery plaques and IL6 and sIL6R plasma levels correlate moderately with IL6 and sIL6R. Our data suggest that IL6 signaling in the circulation might mirror the system activity in the plaque, thus adding novel perspectives to the role of IL6 signaling in atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2021
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32. Genetic Susceptibility Loci for Cardiovascular Disease and Their Impact on Atherosclerotic Plaques

Author

Circulatory Health, Experimentele Afd. Cardiologie 1, CDL Arcadia, MDL onderzoek 1, Onderzoek, Child Health, Device, Onderzoek Precision medicine, Gipskamer Chirurgie, Zorgeenheid Vaatchirurgie Medisch, Brain, Cardiovasculaire Epi Team 7a, CMM Groep Kaaij, Divisie Biomedische Genetica, CDL Onderzoek Pasterkamp, Divisie LAB, van der Laan, Sander W., Siemelink, Marten A., Haitjema, Saskia, Foroughi Asl, Hassan, Perisic, Ljubica, Mokry, Michal, van Setten, Jessica, Malik, Rainer, Dichgans, Martin, Worrall, Bradford B., Samani, Nilesh J., Schunkert, Heribert, Erdmann, Jeanette, Hedin, Ulf, Paulsson-Berne, Gabrielle, Björkegrenn, Johan L.M., de Borst, Gert J., Asselbergs, Folkert W., den Ruijter, Folkert W., de Bakker, Paul I.W., Pasterkamp, Gerard, METASTROKE Collaboration of the International Stroke Genetics Consortium, Circulatory Health, Experimentele Afd. Cardiologie 1, CDL Arcadia, MDL onderzoek 1, Onderzoek, Child Health, Device, Onderzoek Precision medicine, Gipskamer Chirurgie, Zorgeenheid Vaatchirurgie Medisch, Brain, Cardiovasculaire Epi Team 7a, CMM Groep Kaaij, Divisie Biomedische Genetica, CDL Onderzoek Pasterkamp, Divisie LAB, van der Laan, Sander W., Siemelink, Marten A., Haitjema, Saskia, Foroughi Asl, Hassan, Perisic, Ljubica, Mokry, Michal, van Setten, Jessica, Malik, Rainer, Dichgans, Martin, Worrall, Bradford B., Samani, Nilesh J., Schunkert, Heribert, Erdmann, Jeanette, Hedin, Ulf, Paulsson-Berne, Gabrielle, Björkegrenn, Johan L.M., de Borst, Gert J., Asselbergs, Folkert W., den Ruijter, Folkert W., de Bakker, Paul I.W., Pasterkamp, Gerard, and METASTROKE Collaboration of the International Stroke Genetics Consortium

Published
2018

33. Integrated Human Evaluation of the Lysophosphatidic Acid Pathway as a Novel Therapeutic Target in Atherosclerosis

Author

Aldi, Silvia, primary, Matic, Ljubica Perisic, additional, Hamm, Gregory, additional, van Keulen, Daniëlle, additional, Tempel, Dennie, additional, Holmstrøm, Kim, additional, Szwajda, Agnieszka, additional, Nielsen, Boye Schnack, additional, Emilsson, Valur, additional, Ait-Belkacem, Rima, additional, Lengquist, Mariette, additional, Paulsson-Berne, Gabrielle, additional, Eriksson, Per, additional, Lindeman, Jan H.N., additional, Gool, Alain J., additional, Stauber, Jonathan, additional, Hedin, Ulf, additional, and Hurt-Camejo, Eva, additional

Published
2018
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35. Abstract 627: Combined Plaque Evaluation by Ultrasound and Microarrays Reveals Bclaf1 as a Novel Regulator of Smooth Muscle Cell Transdifferentiation in Atherosclerosis

Author

Rykaczewska, Urszula, primary, Saliba-Gustafsson, Peter, additional, Lengquist, Mariette, additional, Kronqvist, Malin, additional, Lund, Kent, additional, Caidahl, Kenneth, additional, Skogsberg, Josefin, additional, Vukojevic, Vladana, additional, Lindeman, Jan H, additional, Paulsson-Berne, Gabrielle, additional, Hansson, Göran K, additional, Leeper, Nicholas, additional, Ehrenborg, Ewa, additional, Razuvaev, Anton, additional, Hedin, Ulf, additional, and Perisic Matic, Ljubica, additional

Published
2018
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36. Altered metabolism distinguishes high-risk from stable carotid atherosclerotic plaques

Author

Tomas, Lukas, primary, Edsfeldt, Andreas, additional, Mollet, Inês G, additional, Perisic Matic, Ljubica, additional, Prehn, Cornelia, additional, Adamski, Jerzy, additional, Paulsson-Berne, Gabrielle, additional, Hedin, Ulf, additional, Nilsson, Jan, additional, Bengtsson, Eva, additional, Gonçalves, Isabel, additional, and Björkbacka, Harry, additional

Published
2018
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38. Abstract 95: MiRNA-210 Enhances Fibrous Cap Stability in Advanced Atherosclerotic Lesions

Author

Eken, Suzanne M, primary, Jin, Hong, additional, Chernogubova, Ekaterina, additional, Li, Yuhuang, additional, Simon, Nancy, additional, Sun, Changyan, additional, Korzunowicz, Greg, additional, Busch, Albert, additional, Bäcklund, Alexandra, additional, Österholm, Cecilia, additional, Razuvaev, Anton, additional, Renné, Thomas, additional, Eckstein, Hans H, additional, Pelisek, Jaroslav, additional, Eriksson, Per, additional, Gonzalez Diez, Maria, additional, Matic Perisic, Ljubica, additional, Schellinger, Isabel N, additional, Raaz, Uwe, additional, Leeper, Nicholas J, additional, Hansson, Göran K, additional, Paulsson-Berne, Gabrielle, additional, Hedin, Ulf, additional, and Maegdefessel, Lars, additional

Published
2017
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39. Abstract 23: Identification of NCF4 as a Novel Regulator in Arterial Remodeling and Advanced Atherosclerosis

Author

Bäcklund, Alexandra, primary, Gertow, Karl, additional, Jin, Hong, additional, Olsson, Lina, additional, Gonzalez-Diez, Maria, additional, Sabater-Lleal, Maria, additional, Strawbridge, Rona J, additional, Sennblad, Bengt, additional, Öhrvik, John, additional, Zabaneh, Delilah, additional, Shah, Sonia, additional, Veglia, Fabrizio, additional, Folkersen, Lasse, additional, Gigante, Bruna, additional, Leander, Karin, additional, Vikström, Max, additional, Silveira, Angela, additional, Colombo, Gualtiero I, additional, Gabrielsen, Anders, additional, Hedin, Ulf, additional, Franco-Cereceda, Anders, additional, Paulsson-Berne, Gabrielle, additional, Nyyssönen, Kristiina, additional, Tuomainen, Tomi-pekka, additional, Savonen, Kai, additional, Rauramaa, Rainer, additional, Smit, Andries J, additional, Giral, Philippe, additional, Mannarino, Elmo, additional, van der Laan, Sander W, additional, Pasterkamp, Gerard, additional, Hansson, Göran K, additional, Eriksson, Per, additional, Baldassarre, Damiano, additional, Tremoli, Elena, additional, de Faire, Ulf, additional, Humphries, Steve E, additional, Hamsten, Anders, additional, Holmdahl, Rikard, additional, and Maegdefessel, Lars, additional

Published
2017
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40. Abstract 219: Deficiency of the T Cell Regulator Cbl-B Aggravates Atherosclerosis by Inducing CD8 + T Cell-Mediated Macrophage Death

Author

Seijkens, Tom T, primary, Winkels, Holger, additional, Gijbels, Marion, additional, Kuivenhoven, Jan A, additional, Perisic, Ljubica, additional, Paulsson-Berne, Gabrielle, additional, Hedin, Ulf, additional, Hansson, Goran K, additional, Weber, Christian, additional, Gerdes, Norbert, additional, de Winther, Menno P, additional, and Lutgens, Esther, additional

Published
2017
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42. Deficiency of the T cell regulator Casitas B-cell lymphoma-B aggravates atherosclerosis by inducing CD8 + T cell-mediated macrophage death.

Author

Seijkens, Tom T P, Poels, Kikkie, Meiler, Svenja, Tiel, Claudia M van, Kusters, Pascal J H, Reiche, Myrthe, Atzler, Dorothee, Winkels, Holger, Tjwa, Marc, Poelman, Hessel, Slütter, Bram, Kuiper, Johan, Gijbels, Marion, Kuivenhoven, Jan Albert, Matic, Ljubica Perisic, Paulsson-Berne, Gabrielle, Hedin, Ulf, Hansson, Göran K, Nicolaes, Gerry A F, and Daemen, Mat J A P

Abstract

Aims The E3-ligase CBL-B (Casitas B-cell lymphoma-B) is an important negative regulator of T cell activation that is also expressed in macrophages. T cells and macrophages mediate atherosclerosis, but their regulation in this disease remains largely unknown; thus, we studied the function of CBL-B in atherogenesis. Methods and results The expression of CBL-B in human atherosclerotic plaques was lower in advanced lesions compared with initial lesions and correlated inversely with necrotic core area. Twenty weeks old Cblb−/−Apoe−/− mice showed a significant increase in plaque area in the aortic arch, where initial plaques were present. In the aortic root, a site containing advanced plaques, lesion area rose by 40%, accompanied by a dramatic change in plaque phenotype. Plaques contained fewer macrophages due to increased apoptosis, larger necrotic cores, and more CD8+ T cells. Cblb−/−Apoe−/− macrophages exhibited enhanced migration and increased cytokine production and lipid uptake. Casitas B-cell lymphoma-B deficiency increased CD8+ T cell numbers, which were protected against apoptosis and regulatory T cell-mediated suppression. IFNγ and granzyme B production was enhanced in Cblb−/−Apoe−/− CD8+ T cells, which provoked macrophage killing. Depletion of CD8+ T cells in Cblb−/−Apoe−/− bone marrow chimeras rescued the phenotype, indicating that CBL-B controls atherosclerosis mainly through its function in CD8+ T cells. Conclusion Casitas B-cell lymphoma-B expression in human plaques decreases during the progression of atherosclerosis. As an important regulator of immune responses in experimental atherosclerosis, CBL-B hampers macrophage recruitment and activation during initial atherosclerosis and limits CD8+ T cell activation and CD8+ T cell-mediated macrophage death in advanced atherosclerosis, thereby preventing the progression towards high-risk plaques. View large Download slide View large Download slide [ABSTRACT FROM AUTHOR]

Published
2019
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43. Low TLR7 gene expression in atherosclerotic plaques is associated with major adverse cardio- and cerebrovascular events

Author

Karadimou, Glykeria, Folkersen, Lasse, Berg, Martin, Perisic, Ljubica, Discacciati, Andrea, Roy, Joy, Hansson, Göran K, Persson, Jonas, Paulsson-Berne, Gabrielle, Karadimou, Glykeria, Folkersen, Lasse, Berg, Martin, Perisic, Ljubica, Discacciati, Andrea, Roy, Joy, Hansson, Göran K, Persson, Jonas, and Paulsson-Berne, Gabrielle

Abstract

Aims: Processes in the development of atherosclerotic lesions can lead to plaque rupture or erosion, which can in turn elicit myocardial infarction or ischaemic stroke. The aims of this study were to determine whether Toll-like receptor 7 (TLR7) gene expression levels influence patient outcome and to explore the mechanisms linked to TLR7 expression in atherosclerosis. Methods and Results: Atherosclerotic plaques were removed by carotid endarterectomy (CEA) and subjected to gene array expression analysis (n=123). Increased levels of TLR7 transcript in the plaques were associated with better outcome in a follow-up study over a maximum of 8 years. Patients with higher TLR7 transcript levels had a lower risk of experiencing major cardiovascular and cerebrovascular events (MACCE) during the follow-up period after CEA (hazard ratio: 2.38, p=0.012, 95% CI 1.21-4.67). TLR7 was expressed in all plaques by T cells, macrophages and endothelial cells in capillaries, as shown by immunohistochemistry. In short-term tissue cultures, ex vivo treatment of plaques with the TLR7 ligand imiquimod elicited dose-dependent secretion of IL-10, TNF-α, GM-CSF, and IL-12/IL-23p40. This secretion was blocked with a TLR7 inhibitor. Immunofluorescent tissue analysis after TLR7 stimulation showed IL-10 expression in T cells, macrophages and vascular smooth muscle cells. TLR7 mRNA levels in the plaques were correlated with IL-10 receptor (r=0.4031, p<0.0001) and GM-CSF receptor A (r=0.4354, p<0.0001) transcripts.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Conclusions These findings demonstrate that TLR7 is abundantly expressed in human atherosclerotic plaques. TLR7 ligation eli

Published
2016

44. Abstract 173: Proprotein Convertase Subtilisin/Kexin Type 6 is a Key Protease in the Control of Smooth Muscle Cell Function in Vascular Disease

Author

Hedin, Ulf, primary, Perisic, Ljubica, additional, Rykaczewska, Urszula, additional, Razuvaev, Anton, additional, Lengquist, Mariette, additional, Sabater-Lleal, Maria, additional, Eriksson, Ida, additional, Röhl, Samuel, additional, Kronqvist, Malin, additional, Tseng, Chi-Nan, additional, Rodriguez, Patricia, additional, Folkersen, Lasse, additional, Du, Lei, additional, Gonzalez Diez, Maria, additional, Osterholm, Cecilia, additional, Roy, Joy, additional, Patrakka, Jaakko, additional, Paulsson-Berne, Gabrielle, additional, Hansson, Göran, additional, Odeberg, Jacob, additional, Hamsten, Anders, additional, and Eriksson, Per, additional

Published
2016
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46. Abstract 512: The Long Non-coding Rna MIAT Regulates Smooth Muscle Cell Proliferation and Macrophage Activity in Advanced Atherosclerotic Lesions

Author

Li, Yuhuang, primary, Jin, Hong, additional, Perisic, Ljubica, additional, Chernogubova, Ekaterina, additional, Bäcklund, Alexandra, additional, Gustafsson, Peter, additional, Werngren, Olivera, additional, Busch, Albert, additional, Eken, Suzanne, additional, Sun, Changyan, additional, Hansson, Göran K, additional, Paulsson-Berne, Gabrielle, additional, Hedin, Ulf, additional, Bergmark, Claes, additional, and Maegdefessel, Lars, additional

Published
2016
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47. Abstract 127: Induction of miR-21 Increases Fibrous Cap Stability in Vulnerable Atherosclerotic Lesions

Author

Jin, Hong, primary, Li, Yuhuang, additional, Bäcklund, Alexandra, additional, Busch, Albert, additional, Eken, Suzanne M, additional, Chernogubova, Ekaterina, additional, Gustafsson, Peter, additional, Perisic, Ljubica, additional, Schellinger, Isabel, additional, Raaz, Uwe, additional, Tsao, Philip S, additional, Hansson, Göran K, additional, Paulsson- Berne, Gabrielle, additional, Hedin, Ulf, additional, and Maegdefessel, Lars, additional

Published
2016
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49. Abstract 367: Pcsk6 Is a Key Protease Modulating Smooth Muscle Cell Activation in Vascular Remodeling and Plaque Vulnerability

Author

Perisic Matic, Ljubica, primary, Razuvaev, Anton, additional, Lengquist, Mariette, additional, Sabater-Lleal, Maria, additional, Folkersen, Lasse, additional, Du, Lei, additional, Österholm, Cecilia, additional, Roy, Joy, additional, Kronqvist, Malin, additional, Frebelius, Siw, additional, Gonzalez Diez, Maria, additional, Hedin, Erika, additional, Paulsson-Berne, Gabrielle, additional, Hansson, Göran K, additional, Odeberg, Jacob, additional, Hamsten, Anders, additional, Eriksson, Per, additional, and Hedin, Ulf, additional

Published
2015
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50. Abstract 150: Identification of SYNPO2, SYNM, LMOD1, PDLIM7 and PLN as Novel Markers of Smooth Muscle Cells in Atherosclerosis

Author

Hedin, Ulf, primary, Perisic Matic, Ljubica, additional, Razuvaev, Anton, additional, Sabater-Lleal, Maria, additional, Lengquist, Mariette, additional, Miller, Clint L, additional, Roy, Joy, additional, Kronqvist, Malin, additional, Gonzalez Diez, Maria, additional, Frebelius, Siw, additional, Leeper, Nick, additional, Maegdefessel, Lars, additional, Quertermous, Thomas, additional, Paulsson-Berne, Gabrielle, additional, Odeberg, Jacob, additional, Hansson, Göran K, additional, and Hamsten, Anders, additional

Published
2015
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