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  Lineage tracing of cells involved in atherosclerosis

Albarran Juarez, J. A., Kaur, H., Grimm, M., Offermanns, S., & Wettschureck, N. (2016). Lineage tracing of cells involved in atherosclerosis. ATHEROSCLEROSIS, 251, 445-453. doi:10.1016/j.atherosclerosis.2016.06.012.

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 Creators:
Albarran Juarez, Julian Alberto1, Author              
Kaur, Harmandeep1, Author              
Grimm, Myriam1, Author              
Offermanns, Stefan1, Author              
Wettschureck, Nina1, Author              
Affiliations:
1Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              

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Free keywords: SMOOTH-MUSCLE-CELLS; MACROPHAGE-LIKE CELLS; GENE; MOUSE; TRANSDIFFERENTIATION; ATHEROGENESIS; GRANULOCYTES; PATHOGENESIS; EXPRESSION; LESIONSCardiovascular System & Cardiology; Atherosclerosis; Lineage tracing; Gene expression; Smooth muscle cell; Macrophage; Transdifferentiation;
 Abstract: Background and aims: Despite the clinical importance of atherosclerosis, the origin of cells within atherosclerotic plaques is not fully understood. Due to the lack of a definitive lineage-tracing strategy, previous studies have provided controversial results about the origin of cells expressing smooth muscle and macrophage markers in atherosclerosis. We here aim to identify the origin of vascular smooth muscle (SM) cells and macrophages within atherosclerosis lesions. Methods: We combined a genetic fate mapping approach with single cell expression analysis in a murine model of atherosclerosis. Results: We found that 16% of CD68-positive plaque macrophage-like cells were derived from mature SM cells and not from myeloid sources, whereas 31% of alpha SMA-positive smooth muscle-like cells in plaques were not SM-derived. Further analysis at the single cell level showed that SM-derived CD68(+) cells expressed higher levels of inflammatory markers such as cyclooxygenase 2 (Ptgs2, p = 0.02), and vascular cell adhesion molecule (Vcam1, p = 0.05), as well as increased mRNA levels of genes related to matrix synthesis such as Col1a2 (p = 0.01) and Fn1 (p = 0.04), than non SM-derived CD68(+) cells. Conclusions: These results demonstrate that smooth muscle cells within atherosclerotic lesions can switch to a macrophage-like phenotype characterized by higher expression of inflammatory and synthetic markers genes that may further contribute to plaque progression. (C) 2016 The Authors. Published by Elsevier Ireland Ltd.

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Language(s): eng - English
 Dates: 2016
 Publication Status: Published in print
 Pages: 9
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
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Title: ATHEROSCLEROSIS
Source Genre: Journal
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Publ. Info: ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND : ELSEVIER IRELAND LTD
Pages: - Volume / Issue: 251 Sequence Number: - Start / End Page: 445 - 453 Identifier: ISSN: 0021-9150