Author
Listed:
- Simon Renders
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH)
Heidelberg University Hospital)
- Arthur Flohr Svendsen
(University Medical Center Groningen, University of Groningen)
- Jasper Panten
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH)
Heidelberg University)
- Nicolas Rama
(Centre Léon Bérard)
- Maria Maryanovich
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Pia Sommerkamp
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH)
Heidelberg University)
- Luisa Ladel
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH))
- Anna Rita Redavid
(Centre Léon Bérard)
- Benjamin Gibert
(Centre Léon Bérard)
- Seka Lazare
(University Medical Center Groningen, University of Groningen)
- Benjamin Ducarouge
(Centre Léon Bérard)
- Katharina Schönberger
(Max Planck Institute of Immunobiology and Epigenetics)
- Andreas Narr
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH)
Heidelberg University)
- Manon Tourbez
(University Medical Center Groningen, University of Groningen)
- Bertien Dethmers-Ausema
(University Medical Center Groningen, University of Groningen)
- Erik Zwart
(University Medical Center Groningen, University of Groningen)
- Agnes Hotz-Wagenblatt
(German Cancer Research Center (DKFZ))
- Dachuan Zhang
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Claudia Korn
(University of Cambridge
University of Cambridge
NHS Blood and Transplant)
- Petra Zeisberger
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH))
- Adriana Przybylla
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH))
- Markus Sohn
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH))
- Simon Mendez-Ferrer
(University of Cambridge
University of Cambridge
NHS Blood and Transplant)
- Mathias Heikenwälder
(German Cancer Research Center Heidelberg (DKFZ))
- Maik Brune
(Heidelberg University Hospital)
- Daniel Klimmeck
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH))
- Leonid Bystrykh
(University Medical Center Groningen, University of Groningen)
- Paul S. Frenette
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Patrick Mehlen
(Centre Léon Bérard)
- Gerald de Haan
(University Medical Center Groningen, University of Groningen)
- Nina Cabezas-Wallscheid
(Max Planck Institute of Immunobiology and Epigenetics)
- Andreas Trumpp
(German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance
Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH)
German Cancer Consortium (DKTK))
Abstract
Haematopoietic stem cells (HSCs) are characterized by their self-renewal potential associated to dormancy. Here we identify the cell surface receptor neogenin-1 as specifically expressed in dormant HSCs. Loss of neogenin-1 initially leads to increased HSC expansion but subsequently to loss of self-renewal and premature exhaustion in vivo. Its ligand netrin-1 induces Egr1 expression and maintains quiescence and function of cultured HSCs in a Neo1 dependent manner. Produced by arteriolar endothelial and periarteriolar stromal cells, conditional netrin-1 deletion in the bone marrow niche reduces HSC numbers, quiescence and self-renewal, while overexpression increases quiescence in vivo. Ageing associated bone marrow remodelling leads to the decline of netrin-1 expression in niches and a compensatory but reversible upregulation of neogenin-1 on HSCs. Our study suggests that niche produced netrin-1 preserves HSC quiescence and self-renewal via neogenin-1 function. Decline of netrin-1 production during ageing leads to the gradual decrease of Neo1 mediated HSC self-renewal.
Suggested Citation
Simon Renders & Arthur Flohr Svendsen & Jasper Panten & Nicolas Rama & Maria Maryanovich & Pia Sommerkamp & Luisa Ladel & Anna Rita Redavid & Benjamin Gibert & Seka Lazare & Benjamin Ducarouge & Katha, 2021.
"Niche derived netrin-1 regulates hematopoietic stem cell dormancy via its receptor neogenin-1,"
Nature Communications, Nature, vol. 12(1), pages 1-15, December.
Handle:
RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-020-20801-0
DOI: 10.1038/s41467-020-20801-0
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Cited by:
- Pradeep Ramalingam & Michael C. Gutkin & Michael G. Poulos & Taylor Tillery & Chelsea Doughty & Agatha Winiarski & Ana G. Freire & Shahin Rafii & David Redmond & Jason M. Butler, 2023.
"Restoring bone marrow niche function rejuvenates aged hematopoietic stem cells by reactivating the DNA Damage Response,"
Nature Communications, Nature, vol. 14(1), pages 1-20, December.
- Benjamin B. Sun & Stephanie J. Loomis & Fabrizio Pizzagalli & Natalia Shatokhina & Jodie N. Painter & Christopher N. Foley & Megan E. Jensen & Donald G. McLaren & Sai Spandana Chintapalli & Alyssa H. , 2022.
"Genetic map of regional sulcal morphology in the human brain from UK biobank data,"
Nature Communications, Nature, vol. 13(1), pages 1-13, December.
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