Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/117154
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chen, X. | - |
dc.contributor.author | Deng, H. | - |
dc.contributor.author | Churchill, M. | - |
dc.contributor.author | Luchsinger, L. | - |
dc.contributor.author | Du, X. | - |
dc.contributor.author | Chu, T. | - |
dc.contributor.author | Friedman, R. | - |
dc.contributor.author | Middelhoff, M. | - |
dc.contributor.author | Ding, H. | - |
dc.contributor.author | Tailor, Y. | - |
dc.contributor.author | Wang, A. | - |
dc.contributor.author | Liu, H. | - |
dc.contributor.author | Niu, Z. | - |
dc.contributor.author | Wang, H. | - |
dc.contributor.author | Jiang, Z. | - |
dc.contributor.author | Renders, S. | - |
dc.contributor.author | Ho, S. | - |
dc.contributor.author | Shah, S. | - |
dc.contributor.author | Tishchenko, P. | - |
dc.contributor.author | Chang, W. | - |
dc.contributor.author | et al. | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Cell Stem Cell, 2017; 21(6):747-760 | - |
dc.identifier.issn | 1934-5909 | - |
dc.identifier.issn | 1875-9777 | - |
dc.identifier.uri | http://hdl.handle.net/2440/117154 | - |
dc.description.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. | - |
dc.description.statementofresponsibility | Xiaowei Chen ... Daniel L. Worthley ... et al. | - |
dc.language.iso | en | - |
dc.publisher | Elsevier | - |
dc.rights | Copyright status unknown | - |
dc.source.uri | http://dx.doi.org/10.1016/j.stem.2017.11.003 | - |
dc.subject | H2 receptor; bone marrow niche; hematopoietic stem cells; histamine; myeloid biased | - |
dc.title | Bone marrow myeloid cells regulate myeloid-biased hematopoietic stem cells via a histamine-dependent feedback loop | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1016/j.stem.2017.11.003 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Worthley, D. [0000-0003-0374-9124] | - |
Appears in Collections: | Aurora harvest 3 Medicine publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.