Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed‐forward loop between LXR and autophagy
Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin‐2 reduces plasma triglycerides and may therefore be beneficial to reduce a...
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| Veröffentlicht in: | Journal of internal medicine Jg. 286; H. 6; S. 660 - 675 |
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| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
England
Blackwell Publishing Ltd
01.12.2019
Wiley John Wiley and Sons Inc |
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| ISSN: | 0954-6820, 1365-2796, 1365-2796 |
| Online-Zugang: | Volltext |
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| Abstract | Background
Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin‐2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development.
Objective
We sought to delineate putative beneficial effects of the Pro251 variant of perlipin‐2 on subclinical atherosclerosis and the mechanism by which it acts.
Methods
A pan‐European cohort of high‐risk individuals where carotid intima‐media thickness has been assessed was adopted. Human primary monocyte‐derived macrophages were prepared from whole blood from individuals recruited by perilipin‐2 genotype or from buffy coats from the Karolinska University hospital blood central.
Results
The Pro251 variant of perilipin‐2 is associated with decreased intima‐media thickness at baseline and over 30 months of follow‐up. Using human primary monocyte‐derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver‐X‐receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed‐forward loop, regulated by CYP27A1 and 27OH‐cholesterol.
Conclusions
For the first time, we show that perilipin‐2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin‐2 modulates levels of the LXR ligand 27OH‐cholesterol and initiates a feed‐forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin‐2 exerts its beneficial effects on subclinical atherosclerosis. |
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| AbstractList | Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development.BACKGROUNDHyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development.We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts.OBJECTIVEWe sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts.A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central.METHODSA pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central.The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol.RESULTSThe Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol.For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis.CONCLUSIONSFor the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis. Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts. A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central. The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol. For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis. BackgroundHyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin‐2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development.ObjectiveWe sought to delineate putative beneficial effects of the Pro251 variant of perlipin‐2 on subclinical atherosclerosis and the mechanism by which it acts.MethodsA pan‐European cohort of high‐risk individuals where carotid intima‐media thickness has been assessed was adopted. Human primary monocyte‐derived macrophages were prepared from whole blood from individuals recruited by perilipin‐2 genotype or from buffy coats from the Karolinska University hospital blood central.ResultsThe Pro251 variant of perilipin‐2 is associated with decreased intima‐media thickness at baseline and over 30 months of follow‐up. Using human primary monocyte‐derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver‐X‐receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed‐forward loop, regulated by CYP27A1 and 27OH‐cholesterol.ConclusionsFor the first time, we show that perilipin‐2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin‐2 modulates levels of the LXR ligand 27OH‐cholesterol and initiates a feed‐forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin‐2 exerts its beneficial effects on subclinical atherosclerosis. Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin‐2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. Objective We sought to delineate putative beneficial effects of the Pro251 variant of perlipin‐2 on subclinical atherosclerosis and the mechanism by which it acts. Methods A pan‐European cohort of high‐risk individuals where carotid intima‐media thickness has been assessed was adopted. Human primary monocyte‐derived macrophages were prepared from whole blood from individuals recruited by perilipin‐2 genotype or from buffy coats from the Karolinska University hospital blood central. Results The Pro251 variant of perilipin‐2 is associated with decreased intima‐media thickness at baseline and over 30 months of follow‐up. Using human primary monocyte‐derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver‐X‐receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed‐forward loop, regulated by CYP27A1 and 27OH‐cholesterol. Conclusions For the first time, we show that perilipin‐2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin‐2 modulates levels of the LXR ligand 27OH‐cholesterol and initiates a feed‐forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin‐2 exerts its beneficial effects on subclinical atherosclerosis. Background: Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. Objective: We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts. Methods: A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central. Results: The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol. Conclusions: For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis. Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. Objective We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts. Methods A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central. Results The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol. Conclusions For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis. |
| Author | Hamsten, A. Discacciati, A. Janas, V. Franco‐Cereceda, A. Cooper, J. Tuomainen, T. P. Ahl, M. Blomgren, G. van Roon, A. M. Kahn, J. F. Eriksson, M. J. Bilo, H. J. G. Kontush, A. Vaudo, G. Nyyssonen, K. Mulder, D. J. Smeets, G. H. Pirro, M. Rauramaa, E. Siepi, D. Baldassarre, D. Gessel, A. I. Kuipers, W. D. Karppi, J. Haarsma‐Jorritsma, P. Carreau, V. Borén, J. Faire, U. Bruin, M. Orho‐Melander, M. Sirtori, C. R. Beaudeux, J. L. Humphries, S.E. Kurl, S. Parini, P. Ehrenborg, E. Nurmi, T. Penttila, I. M. Tremoli, E. Pedrelli, M. Saliba‐Gustafsson, P. Nilson, L. Huttunen, K. Giral, P. Nicolai, A. Gonçalves, I. Teune, G. C. Alaeddin, A. Fahlstadius, P. Castelnuovo, S. Eriksson, P. Bovis, F. Veglia, F. Torronen, J. Sansaro, D. Amato, M. Gertow, K. Smit, A.J. Werngren, O. Magné, J. Pekkarinen, H. Rauramaa, R. Schillaci, G. Tedesco, C. Frigerio, B. Salonen, R. Acharya, J. Pourteymour, S. Tuomainen, J. Ravani, A. Heinonen, M. Kauhanen, J. Lupattelli, G. |
| AuthorAffiliation | 9 Assistance Publique Hopitaux de Paris, Service Endocrinologie‐Metabolisme, Groupe Hospitalier Pitie‐Salpetriere Unites de Prevention Cardiovasculaire Paris France 10 Institute of Public Health and Clinical Nutrition University of Eastern Finland Kuopio Finland 1 Cardiovascular Medicine Unit, Department of Medicine, Center for Molecular Medicine at BioClinicum Karolinska University Hospital, Karolinska Institutet Stockholm Sweden 14 Experimental Cardiovascular Research Group and Cardiology Department, Clinical Research Center, Clinical Sciences Malmö Lund University Lund Sweden 8 Department of Medicine University Medical Center Groningen Groningen The Netherlands 17 Department of Molecular and Clinical Medicine/Wallenberg Laboratory University of Gothenburg and Sahlgrenska University Hospital Gothenburg Sweden 18 St Jude Children’s Research Hospital Department of Immunology Memphis Tennessee USA 19 Metabolism Unit, Department of Medicine Karolinska Institutet at Karolinska University Hospita |
| AuthorAffiliation_xml | – name: 7 Foundation for Research in Health Exercise and Nutrition Kuopio Research Institute of Exercise Medicine Kuopio Finland – name: 2 Cardiovascular Medicine Stanford University School of Medicine Palo Alto California USA – name: 3 Division of Clinical Chemistry, Department of Laboratory Medicine Karolinska Institutet Huddinge Huddinge Sweden – name: 12 Division of Cardiovascular Epidemiology, Institute of Environmental Medicine Karolinska Institutet Stockholm Sweden – name: 8 Department of Medicine University Medical Center Groningen Groningen The Netherlands – name: 11 Unit of Internal Medicine, Angiology and Arteriosclerosis Diseases, Department of Medicine University of Perugia Perugia Italy – name: 1 Cardiovascular Medicine Unit, Department of Medicine, Center for Molecular Medicine at BioClinicum Karolinska University Hospital, Karolinska Institutet Stockholm Sweden – name: 10 Institute of Public Health and Clinical Nutrition University of Eastern Finland Kuopio Finland – name: 5 Centro Cardiologico Monzino, IRCCS Milan Italy – name: 18 St Jude Children’s Research Hospital Department of Immunology Memphis Tennessee USA – name: 14 Experimental Cardiovascular Research Group and Cardiology Department, Clinical Research Center, Clinical Sciences Malmö Lund University Lund Sweden – name: 16 Cardiothoracic Surgery Unit, Department of Molecular Medicine and Surgery Karolinska Institutet at Karolinska University Hospital Solna Solna Sweden – name: 6 Dipartimento di Scienze Farmacologiche e Biomolecolari Università di Milano Milan Italy – name: 4 Department of Medical Biotechnology and Translational Medicine Università degli Studi di Milano Milan Italy – name: 15 Department of Clinical Sciences in Malmö, Lund University Diabetes Centre Lund University Lund Sweden – name: 19 Metabolism Unit, Department of Medicine Karolinska Institutet at Karolinska University Hospital Huddinge Huddinge Sweden – name: 13 Centre for Cardiovascular Genetics, Institute Cardiovascular Science University College London London UK – name: 9 Assistance Publique Hopitaux de Paris, Service Endocrinologie‐Metabolisme, Groupe Hospitalier Pitie‐Salpetriere Unites de Prevention Cardiovasculaire Paris France – name: 17 Department of Molecular and Clinical Medicine/Wallenberg Laboratory University of Gothenburg and Sahlgrenska University Hospital Gothenburg Sweden |
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| ContentType | Journal Article |
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| Copyright | 2019 The Authors. published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine 2019 The Authors. Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine. Copyright © 2019 The Association for the Publication of the Journal of Internal Medicine Distributed under a Creative Commons Attribution 4.0 International License |
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Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and... Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We... BackgroundHyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and... Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and... Background: Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and... |
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| SubjectTerms | 27OH-cholesterol accumulation Aged Arteriosclerosis Atherosclerosis Atherosclerosis - metabolism Autophagy Blood Buffy coat Cardiology and Cardiovascular Disease Cardiovascular diseases Carotid Intima-Media Thickness Cerebral infarction Cholesterol Clinical Medicine Disease Progression Efflux Europe Female Foam Cells - metabolism General & Internal Medicine Genotypes Health risks Humans Hyperlipidemia identification Inflammation Inflammatory response Kardiologi och kardiovaskulära sjukdomar Klinisk medicin Life Sciences Lipoproteins - metabolism Liver X Receptors - metabolism liver-X-receptor Longitudinal Studies macrophage foam cells Macrophages Macrophages - metabolism Male Medical and Health Sciences Medicin och hälsovetenskap metabolism Middle Aged Monocytes Myocardial infarction Original Perilipin-2 - metabolism Phagocytosis PLIN2 protects receptors reverse cholesterol transport Risk analysis Risk factors ser251pro stimulation Thickness Triglycerides |
| Title | Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed‐forward loop between LXR and autophagy |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjoim.12951 https://www.ncbi.nlm.nih.gov/pubmed/31251843 https://www.proquest.com/docview/2313781663 https://www.proquest.com/docview/2250629298 https://hal.sorbonne-universite.fr/hal-03998908 https://pubmed.ncbi.nlm.nih.gov/PMC6899829 https://gup.ub.gu.se/publication/282972 http://kipublications.ki.se/Default.aspx?queryparsed=id:141456399 |
| Volume | 286 |
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