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Diverse cellular architecture of atherosclerotic plaque derives from clonal expansion of a few medial SMCs

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Authors:
  • Jacobsen, Kevin ;
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    Department of Clinical Medicine - The Department of Cardiological Medicine B, Department of Clinical Medicine, Health, Aarhus University
  • Lund, Marie Bek ;
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    Deparment of Clinical Medicine, Aarhus University, Aarhus, Denmark.
  • Shim, Jeong ;
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    The Department of Cardiological Medicine B, Faculty of Health Sciences, Aarhus University, Aarhus University
  • Gunnersen, Stine ;
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    Department of Clinical Medicine - The Department of Cardiological Medicine B, Department of Clinical Medicine, Health, Aarhus University
  • Füchtbauer, Ernst-Martin ;
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    Department of Molecular Biology and Genetics - Molecular Cell and Developmental Biology, Department of Molecular Biology and Genetics, Science and Technology, Aarhus University
  • Kjolby, Mads ;
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    Department of Biomedicine - Forskning og uddannelse, Vest, Department of Biomedicine, Health, Aarhus University
  • Carramolino, Laura ;
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    Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
  • Bentzon, Jacob Fog
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    Department of Clinical Medicine - The Department of Cardiological Medicine B, Department of Clinical Medicine, Health, Aarhus University
DOI:
10.1172/jci.insight.95890
Abstract:
Fibrous cap smooth muscle cells (SMCs) protect atherosclerotic lesions from rupturing and causing thrombosis, while other plaque SMCs may have detrimental roles in plaque development. To gain insight into recruitment of different plaque SMCs, we mapped their clonal architecture in aggregation chimeras of eGFP+Apoe-/- and Apoe-/- mouse embryos and in mice with a mosaic expression of fluorescent proteins in medial SMCs that were rendered atherosclerotic by PCSK9-induced hypercholesterolemia. Fibrous caps in aggregation chimeras were found constructed from large, endothelial-aligned layers of either eGFP+ or nonfluorescent SMCs, indicating substantial clonal expansion of a few cells. Similarly, plaques in mice with SMC-restricted Confetti expression showed oligoclonal SMC populations with little intermixing between the progeny of different medial SMCs. Phenotypes comprised both ACTA2+ SMCs in the cap and heterogeneous ACTA2- SMCs in the plaque interior, including chondrocyte-like cells and cells with intracellular lipid and crystalline material. Fibrous cap SMCs were invariably arranged in endothelium-aligned clonal sheets, confirming results in the aggregation chimeras. Analysis of the clonal structure showed that a low number of local medial SMCs partake in atherosclerosis and that single medial SMCs can produce several different SMC phenotypes in plaque. The combined results show that few medial SMCs proliferate to form the entire phenotypically heterogeneous plaque SMC population in murine atherosclerosis.
Type:
Journal article
Language:
English
Published in:
Jci Insight, 2017, Vol 2, Issue 19
Main Research Area:
Medical science
Publication Status:
Published
Review type:
Peer Review
Submission year:
2017
Scientific Level:
Scientific
ID:
2391261372

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