Ontogeny of arterial macrophages defines their functions in homeostasis and inflammation

Tobias Weinberger, Dena Esfandyari, Denise Messerer, Gulce Percin, Christian Schleifer, Raffael Thaler, Lulu Liu, Christopher Stremmel, Vanessa Schneider, Ronald J. Vagnozzi, Jennifer Schwanenkamp, Maximilian Fischer, Katrin Busch, Kay Klapproth, Hellen Ishikawa-Ankerhold, Lukas Klösges, Anna Titova, Jeffery D. Molkentin, Yasuhiro Kobayashi, Stefan Engelhardt, Steffen Massberg, Claudia Waskow, Elisa Gomez Perdiguero and Christian Schulz ()
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Tobias Weinberger: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Dena Esfandyari: partner site Munich Heart Alliance
Denise Messerer: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Gulce Percin: Leibniz-Institute on Aging - Fritz-Lipmann-Institute (FLI)
Christian Schleifer: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Raffael Thaler: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Lulu Liu: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Christopher Stremmel: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Vanessa Schneider: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Ronald J. Vagnozzi: Cincinnati Children’s Hospital Medical Center
Jennifer Schwanenkamp: Cincinnati Children’s Hospital Medical Center
Maximilian Fischer: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Katrin Busch: German Cancer Research Center (DKFZ)
Kay Klapproth: German Cancer Research Center (DKFZ)
Hellen Ishikawa-Ankerhold: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Lukas Klösges: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Anna Titova: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Jeffery D. Molkentin: Cincinnati Children’s Hospital Medical Center
Yasuhiro Kobayashi: Matsumoto Dental University
Stefan Engelhardt: partner site Munich Heart Alliance
Steffen Massberg: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität
Claudia Waskow: Leibniz-Institute on Aging - Fritz-Lipmann-Institute (FLI)
Elisa Gomez Perdiguero: Département de Biologie du Développement et Cellules Souches, UMR3738 CNRS
Christian Schulz: Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-Universität

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Arterial macrophages have different developmental origins, but the association of macrophage ontogeny with their phenotypes and functions in adulthood is still unclear. Here, we combine macrophage fate-mapping analysis with single-cell RNA sequencing to establish their cellular identity during homeostasis, and in response to angiotensin-II (AngII)-induced arterial inflammation. Yolk sac erythro-myeloid progenitors (EMP) contribute substantially to adventitial macrophages and give rise to a defined cluster of resident immune cells with homeostatic functions that is stable in adult mice, but declines in numbers during ageing and is not replenished by bone marrow (BM)-derived macrophages. In response to AngII inflammation, increase in adventitial macrophages is driven by recruitment of BM monocytes, while EMP-derived macrophages proliferate locally and provide a distinct transcriptional response that is linked to tissue regeneration. Our findings thus contribute to the understanding of macrophage heterogeneity, and associate macrophage ontogeny with distinct functions in health and disease.

Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18287-x

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DOI: 10.1038/s41467-020-18287-x

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