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Your search keyword '"Maassen, Sjors"' showing total 2 results
Start Over Author "Maassen, Sjors" Topic atherosclerosis
2 results on '"Maassen, Sjors"'

1. T cell cholesterol efflux suppresses apoptosis and senescence and increases atherosclerosis in middle aged mice.

Author

Bazioti V, La Rose AM, Maassen S, Bianchi F, de Boer R, Halmos B, Dabral D, Guilbaud E, Flohr-Svendsen A, Groenen AG, Marmolejo-Garza A, Koster MH, Kloosterhuis NJ, Havinga R, Pranger AT, Langelaar-Makkinje M, de Bruin A, van de Sluis B, Kohan AB, Yvan-Charvet L, van den Bogaart G, and Westerterp M

Subjects
Animals, Apoptosis, Biological Transport, Immunologic Deficiency Syndromes, Inflammation, Mice, Thymus Gland abnormalities, Atherosclerosis genetics, T-Lymphocytes
Abstract

Atherosclerosis is a chronic inflammatory disease driven by hypercholesterolemia. During aging, T cells accumulate cholesterol, potentially affecting inflammation. However, the effect of cholesterol efflux pathways mediated by ATP-binding cassette A1 and G1 (ABCA1/ABCG1) on T cell-dependent age-related inflammation and atherosclerosis remains poorly understood. In this study, we generate mice with T cell-specific Abca1/Abcg1-deficiency on the low-density-lipoprotein-receptor deficient (Ldlr -/- ) background. T cell Abca1/Abcg1-deficiency decreases blood, lymph node, and splenic T cells, and increases T cell activation and apoptosis. T cell Abca1/Abcg1-deficiency induces a premature T cell aging phenotype in middle-aged (12-13 months) Ldlr -/- mice, reflected by upregulation of senescence markers. Despite T cell senescence and enhanced T cell activation, T cell Abca1/Abcg1-deficiency decreases atherosclerosis and aortic inflammation in middle-aged Ldlr -/- mice, accompanied by decreased T cells in atherosclerotic plaques. We attribute these effects to T cell apoptosis downstream of T cell activation, compromising T cell functionality. Collectively, we show that T cell cholesterol efflux pathways suppress T cell apoptosis and senescence, and induce atherosclerosis in middle-aged Ldlr -/- mice., (© 2022. The Author(s).)

Published
2022
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2. T cell cholesterol efflux suppresses apoptosis and senescence and increases atherosclerosis in middle aged mice

Author

Bazioti, Venetia, La Rose, Anouk M, Maassen, Sjors, Bianchi, Frans, de Boer, Rinse, Halmos, Benedek, Dabral, Deepti, Guilbaud, Emma, Flohr-Svendsen, Arthur, Groenen, Anouk G, Marmolejo-Garza, Alejandro, Koster, Mirjam H, Kloosterhuis, Niels J, Havinga, Rick, Pranger, Alle T, Langelaar-Makkinje, Miriam, de Bruin, Alain, van de Sluis, Bart, Kohan, Alison B, Yvan-Charvet, Laurent, van den Bogaart, Geert, Westerterp, Marit, LS Pathobiologie, Dep Biomolecular Health Sciences, Pathobiologie, dPB RMSC, LS Pathobiologie, Dep Biomolecular Health Sciences, Pathobiologie, dPB RMSC, Molecular Immunology, Molecular Cell Biology, Center for Liver, Digestive and Metabolic Diseases (CLDM), and Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)

Subjects
Inflammation, Multidisciplinary, T-Lymphocytes, Immunologic Deficiency Syndromes, General Physics and Astronomy, Apoptosis, Biological Transport, Thymus Gland, General Chemistry, Atherosclerosis, General Biochemistry, Genetics and Molecular Biology, Mice, Atherosclerosis/genetics, Thymus Gland/abnormalities, Animals
Abstract

Atherosclerosis is a chronic inflammatory disease driven by hypercholesterolemia. During aging, T cells accumulate cholesterol, potentially affecting inflammation. However, the effect of cholesterol efflux pathways mediated by ATP-binding cassette A1 and G1 (ABCA1/ABCG1) on T cell-dependent age-related inflammation and atherosclerosis remains poorly understood. In this study, we generate mice with T cell-specificAbca1/Abcg1-deficiency on the low-density-lipoprotein-receptor deficient (Ldlr−/−) background. T cellAbca1/Abcg1-deficiency decreases blood, lymph node, and splenic T cells, and increases T cell activation and apoptosis. T cellAbca1/Abcg1-deficiency induces a premature T cell aging phenotype in middle-aged (12–13 months)Ldlr−/−mice, reflected by upregulation of senescence markers. Despite T cell senescence and enhanced T cell activation, T cellAbca1/Abcg1-deficiency decreases atherosclerosis and aortic inflammation in middle-agedLdlr−/−mice, accompanied by decreased T cells in atherosclerotic plaques. We attribute these effects to T cell apoptosis downstream of T cell activation, compromising T cell functionality. Collectively, we show that T cell cholesterol efflux pathways suppress T cell apoptosis and senescence, and induce atherosclerosis in middle-agedLdlr−/−mice.

Published
2022

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