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脂蛋白代谢在急性贫血条件下介导造血干细胞反应。

Lipoprotein metabolism mediates hematopoietic stem cell responses under acute anemic conditions.

作者信息

Saito Kiyoka, van der Garde Mark, Umemoto Terumasa, Miharada Natsumi, Sjöberg Julia, Sigurdsson Valgardur, Shirozu Haruki, Kamei Shunsuke, Radulovic Visnja, Suzuki Mitsuyoshi, Nakano Satoshi, Lang Stefan, Hansson Jenny, Olsson Martin L, Minami Takashi, Gouras Gunnar, Flygare Johan, Miharada Kenichi

机构信息

International Research Center for Medical Sciences, Kumamoto University, Kumamoto, Japan.

Division of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.

出版信息

Nat Commun. 2024 Sep 16;15(1):8131. doi: 10.1038/s41467-024-52509-w.

DOI:10.1038/s41467-024-52509-w
PMID:39284836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11405780/
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. VldlrHSCs show higher erythroid potential, which is enhanced after acute anemia induction. VldlrHSCs 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.

摘要

造血干细胞（HSCs）会对各种应激条件做出反应。然而，目前尚不清楚造血干细胞是否以及如何对严重贫血做出反应。在这里，我们证明，在诱导急性贫血后，造血干细胞会迅速增殖并增强其红系分化潜能。在严重贫血时，脂蛋白谱会发生很大变化，载脂蛋白E（ApoE）的浓度会增加。在造血干细胞中，脂质代谢相关基因的转录水平，如极低密度脂蛋白受体（Vldlr），会上调。用ApoE刺激造血干细胞可增强其红系潜能，而Apoe基因敲除小鼠中的造血干细胞对贫血诱导无反应。Vldlr造血干细胞表现出更高的红系潜能，在急性贫血诱导后这种潜能会增强。Vldlr造血干细胞在表观遗传学上是不同的，因为它们的染色质可及性较低，并且在急性贫血诱导后更多的染色质区域会关闭。急性贫血诱导后关闭的染色质区域主要是 Erg 的结合位点。抑制 Erg 可增强造血干细胞的红系分化潜能。我们的研究结果表明，脂蛋白代谢在严重贫血条件下的造血干细胞调节中起着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/5409f3a27a32/41467_2024_52509_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/b456c34b644b/41467_2024_52509_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/b444d6a69ac1/41467_2024_52509_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/5409f3a27a32/41467_2024_52509_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/b456c34b644b/41467_2024_52509_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/e11ba4d3e9a8/41467_2024_52509_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/13ab5f7f1baa/41467_2024_52509_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/b444d6a69ac1/41467_2024_52509_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/ebab0838443b/41467_2024_52509_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/62ad9b3b1a50/41467_2024_52509_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f81/11405780/5409f3a27a32/41467_2024_52509_Fig7_HTML.jpg

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本文引用的文献

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HIF1α-Dependent Induction of by a Combination of Intestinal Inflammation and Systemic Iron Deficiency in Inflammatory Bowel Disease.炎症性肠病中肠道炎症与全身性缺铁共同作用对HIF1α的依赖性诱导作用
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The microbiota regulates hematopoietic stem cell fate decisions by controlling iron availability in bone marrow.
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