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Type: Journal article
Title: Bone marrow myeloid cells regulate myeloid-biased hematopoietic stem cells via a histamine-dependent feedback loop
Author: Chen, X.
Deng, H.
Churchill, M.
Luchsinger, L.
Du, X.
Chu, T.
Friedman, R.
Middelhoff, M.
Ding, H.
Tailor, Y.
Wang, A.
Liu, H.
Niu, Z.
Wang, H.
Jiang, Z.
Renders, S.
Ho, S.
Shah, S.
Tishchenko, P.
Chang, W.
et al.
Citation: Cell Stem Cell, 2017; 21(6):747-760
Publisher: Elsevier
Issue Date: 2017
ISSN: 1934-5909
Statement of
Xiaowei Chen ... Daniel L. Worthley ... et al.
Abstract: Myeloid-biased hematopoietic stem cells (MB-HSCs) play critical roles in recovery from injury, but little is known about how they are regulated within the bone marrow niche. Here we describe an auto-/paracrine physiologic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors marked by histidine decarboxylase (Hdc). Committed Hdc⁺ myeloid cells lie in close anatomical proximity to MB-HSCs and produce histamine, which activates the H₂ receptor on MB-HSCs to promote their quiescence and self-renewal. Depleting histamine-producing cells enforces cell cycle entry, induces loss of serial transplant capacity, and sensitizes animals to chemotherapeutic injury. Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment specifically recruits MB-HSCs and progenitors into the cell cycle; cycling MB-HSCs fail to revert into quiescence in the absence of histamine feedback, leading to their depletion, while an H₂ agonist protects MB-HSCs from depletion after sepsis. Thus, histamine couples lineage-specific physiological demands to intrinsically primed MB-HSCs to enforce homeostasis.
Keywords: H2 receptor; bone marrow niche; hematopoietic stem cells; histamine; myeloid biased
Rights: Copyright status unknown
RMID: 0030082876
DOI: 10.1016/j.stem.2017.11.003
Appears in Collections:Medicine publications

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