Role of Suppressor of Cytokine Signaling-1 In Murine Atherosclerosis
| Autor: | Uwe J. F. Tietge, Silke Glage, Matthias Ballmaier, Karsten Grote, Bernhard Schieffer, Christina Grothusen, Maren Luchtefeld, André Bleich, Harald Schuett, Stefan Lumpe, Anja Hillmer |
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| Přispěvatelé: | Center for Liver, Digestive and Metabolic Diseases (CLDM), Lifestyle Medicine (LM) |
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
Mouse Neutrophils medicine.medical_treatment lcsh:Medicine Suppressor of Cytokine Signaling Proteins MACROPHAGE ACTIVATION PLAQUE DEVELOPMENT SOCS-1 Cardiovascular Immunoenzyme Techniques Antigens Ly Macrophage lcsh:Science Receptor HYPERLIPIDEMIA Mice Knockout Multidisciplinary Animal Models Flow Cytometry Cell biology DNA-Binding Proteins DEFICIENCY medicine.anatomical_structure Cytokine MONOCYTES Cytokines Medicine Female medicine.symptom Signal transduction Signal Transduction Research Article EXPRESSION Immune Cells Inflammation Spleen Biology Diet High-Fat DENSITY-LIPOPROTEIN Suppressor of Cytokine Signaling 1 Protein Model Organisms Vascular Biology medicine Animals Suppressor of cytokine signaling 1 lcsh:R Immunity Dendritic cell Atherosclerosis MICE Receptors LDL Immunology Clinical Immunology lcsh:Q |
| Zdroj: | PLoS ONE, 7(12):e51608. PUBLIC LIBRARY SCIENCE PLoS ONE, Vol 7, Iss 12, p e51608 (2012) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Background: While the impact of inflammation as the substantial driving force of atherosclerosis has been investigated in detail throughout the years, the influence of negative regulators of pro-atherogenic pathways on plaque development has remained largely unknown. Suppressor of cytokine signaling (SOCS)-1 potently restricts transduction of various inflammatory signals and, thereby modulates T-cell development, macrophage activation and dendritic cell maturation. Its role in atherogenesis, however has not been elucidated so far.Methods and Results: Loss of SOCS-1 in the low-density lipoprotein receptor deficient murine model of atherosclerosis resulted in a complex, systemic and ultimately lethal inflammation with increased generation of Ly-6C(hi) monocytes and activated macrophages. Even short-term exposure of these mice to high-cholesterol dieting caused enhanced atherosclerotic plaque development with accumulation of M1 macrophages, Ly-6C positive cells and neutrophils.Conclusion: Our data not only imply that SOCS-1 is athero-protective but also emphasize the fundamental, regulatory importance of SOCS-1 in inflammation-prone organisms. |
| Databáze: | OpenAIRE |
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