Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop
| Autor: | Timothy Chu, C. Benedikt Westphalen, Hans-Willem Snoeck, Haibo Liu, Hongxu Ding, Bernhard W. Renz, Theresa Swayne, Timothy C. Wang, Florence Borot, Michael Churchill, Siddhartha Mukherjee, Simon Renders, Karan Nagar, Daniel L. Worthley, Zhenyu Jiang, Pavel Tishchenko, Alexander L.E. Wang, Laura Munteanu, Andrea Califano, Ryota Takahashi, Moritz Middelhoff, Xing Du, Samuel Asfaha, Yoku Hayakawa, Yagnesh Tailor, Xiaowei Chen, Wenju Chang, Spandan V. Shah, Siu Hong Ho, Chyuan Sheng Lin, Zhengchuan Niu, Richard A. Friedman, Hongshan Wang, Larry L. Luchsinger, Huan Deng |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Myeloid Bone Marrow Cells Biology self-renewal bone marrow niche Article 03 medical and health sciences Paracrine signalling chemistry.chemical_compound Mice Bone Marrow Genetics medicine Animals quiescence Myeloid Cells Progenitor cell myeloid biased histidine decarboxylase Bone Marrow Transplantation hemic and immune systems Cell Biology Flow Cytometry Hematopoietic Stem Cells histamine Histidine decarboxylase hematopoietic stem cells Cell biology Haematopoiesis 030104 developmental biology medicine.anatomical_structure chemistry H2 receptor Molecular Medicine Bone marrow Stem cell Histamine |
| Zdroj: | Paediatrics Publications |
| ISSN: | 1875-9777 |
| Popis: | 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. Chen et al. show that histidine decarboxylase (Hdc) marks quiescent myeloid-biased HSCs (MB-HSCs). Daughter myeloid cells form a spatial cluster with Hdc+ MB-HSCs and secrete histamine to enforce their quiescence and protect them from depletion, following activation by a variety of physiologic insults. |
| Databáze: | OpenAIRE |
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