Lipoprotein metabolism mediates hematopoietic stem cell responses under acute anemic conditions

Kiyoka Saito, Mark Garde, Terumasa Umemoto, Natsumi Miharada, Julia Sjöberg, Valgardur Sigurdsson, Haruki Shirozu, Shunsuke Kamei, Visnja Radulovic, Mitsuyoshi Suzuki, Satoshi Nakano, Stefan Lang, Jenny Hansson, Martin L. Olsson, Takashi Minami, Gunnar Gouras, Johan Flygare and Kenichi Miharada ()
Additional contact information
Kiyoka Saito: Kumamoto University
Mark Garde: Lund University
Terumasa Umemoto: Kumamoto University
Natsumi Miharada: Kumamoto University
Julia Sjöberg: Lund University
Valgardur Sigurdsson: Lund University
Haruki Shirozu: Kumamoto University
Shunsuke Kamei: Kumamoto University
Visnja Radulovic: Lund University
Mitsuyoshi Suzuki: Lund University
Satoshi Nakano: Lund University
Stefan Lang: Lund University
Jenny Hansson: Lund University
Martin L. Olsson: Lund University
Takashi Minami: Kumamoto University
Gunnar Gouras: Lund University
Johan Flygare: Lund University
Kenichi Miharada: Kumamoto University

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Hematopoietic stem cells (HSCs) react to various stress conditions. However, it is unclear whether and how HSCs respond to severe anemia. Here, we demonstrate that upon induction of acute anemia, HSCs rapidly proliferate and enhance their erythroid differentiation potential. In severe anemia, lipoprotein profiles largely change and the concentration of ApoE increases. In HSCs, transcription levels of lipid metabolism-related genes, such as very low-density lipoprotein receptor (Vldlr), are upregulated. Stimulation of HSCs with ApoE enhances their erythroid potential, whereas HSCs in Apoe knockout mice do not respond to anemia induction. VldlrhighHSCs show higher erythroid potential, which is enhanced after acute anemia induction. VldlrhighHSCs are epigenetically distinct because of their low chromatin accessibility, and more chromatin regions are closed upon acute anemia induction. Chromatin regions closed upon acute anemia induction are mainly binding sites of Erg. Inhibition of Erg enhanced the erythroid differentiation potential of HSCs. Our findings indicate that lipoprotein metabolism plays an important role in HSC regulation under severe anemic conditions.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-52509-w Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-52509-w

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-52509-w

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().