Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop

被引：79

作者：

Chen, Xiaowei ^{[1
,2
,3
]}

Deng, Huan ^{[1
,2
,3
,4
,5
]}

Churchill, Michael J. ^{[2
]}

Luchsinger, Larry L. ^{[6
,7
]}

Du, Xing ^{[2
]}

Chu, Timothy H. ^{[1
,3
]}

Friedman, Richard A. ^{[3
,8
,9
]}

Middelhoff, Moritz ^{[1
,3
]}

Ding, Hongxu ^{[8
,9
,10
]}

Tailor, Yagnesh H. ^{[1
,3
]}

Wang, Alexander L. E. ^{[1
,3
]}

Liu, Haibo ^{[1
,3
]}

Niu, Zhengchuan ^{[1
,3
,11
]}

Wang, Hongshan ^{[1
,3
,11
]}

Jiang, Zhenyu ^{[1
,3
]}

Renders, Simon ^{[2
,12
,13
]}

Ho, Siu-Hong ^{[6
]}

Shah, Spandan V. ^{[6
]}

Tishchenko, Pavel ^{[6
]}

Chang, Wenju ^{[1
,3
,11
]}

Swayne, Theresa C. ^{[3
]}

Munteanu, Laura ^{[3
]}

Califano, Andrea ^{[8
,9
,10
]}

Takahashi, Ryota ^{[1
,3
]}

Nagar, Karan K. ^{[1
,3
]}

Renz, Bernhard W. ^{[1
,3
,14
]}

Worthley, Daniel L. ^{[1
,3
,15
,16
]}

Westphalen, C. Benedikt ^{[1
,3
,17
]}

Hayakawa, Yoku ^{[1
,3
,18
]}

Asfaha, Samuel ^{[1
,3
,19
]}

Borot, Florence ^{[2
]}

Lin, Chyuan-Sheng ^{[3
,20
]}

Snoeck, Hans-Willem ^{[6
,7
,21
,22
]}

Mukherjee, Siddhartha ^{[2
]}

Wang, Timothy C. ^{[1
,3
]}

机构：

[1] Columbia Univ, Med Ctr, Div Digest & Liver Dis, Dept Med, New York, NY 10032 USA

[2] Columbia Univ, Med Ctr, Div Hematol Oncol, Dept Med, New York, NY 10032 USA

[3] Columbia Univ, Med Ctr, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA

[4] Nanchang Univ, Dept Pathol, Affiliated Hosp 4, Nanchang 330003, Jiangxi, Peoples R China

[5] Nanchang Univ, Mol Med & Genet Ctr, Affiliated Hosp 4, Nanchang 330003, Jiangxi, Peoples R China

[6] Columbia Univ, Med Ctr, Columbia Ctr Translat Immunol, New York, NY 10032 USA

[7] Columbia Univ, Med Ctr, Ctr Human Dev, New York, NY 10032 USA

[8] Columbia Univ, Med Ctr, Biomed Informat Shared Resource, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA

[9] Columbia Univ, Med Ctr, Dept Biomed Informat, New York, NY 10032 USA

[10] Columbia Univ, Dept Syst Biol, New York, NY 10032 USA

[11] Fudan Univ, Dept Gen Surg, Zhongshan Hosp, Shanghai 200032, Peoples R China

[12] DKFZ ZMBH Alliance, Div Stem Cells & Canc, German Canc Res Ctr DKFZ, D-69120 Heidelberg, Germany

[13] Heidelberg Inst Stem Cell Technol & Expt Med HI S, D-69120 Heidelberg, Germany

[14] Hosp Univ Munich, Dept Gen Visceral & Transplantat Surg, D-81377 Munich, Germany

[15] Univ Adelaide, Sch Med, Adelaide, SA 5005, Australia

[16] SAHMRI, Canc Theme, Adelaide, SA 5005, Australia

[17] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Med 3, D-81377 Munich, Germany

[18] Univ Tokyo, Dept Gastroenterol, Grad Sch Med, Bunkyo Ku, 7-3-1,Hongo, Tokyo 1138655, Japan

[19] Univ Western Ontario, Dept Med, London, ON N6A 5W9, Canada

[20] Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, New York, NY 10032 USA

[21] Columbia Univ, Med Ctr, Dept Med, New York, NY 10032 USA

[22] Columbia Univ, Med Ctr, Dept Microbiol & Immunol, New York, NY 10032 USA

来源：

CELL STEM CELL | 2017年 / 21卷 / 06期

基金：

美国国家科学基金会;

关键词：

PROGENITORS; QUIESCENCE; HETEROGENEITY; INDUCTION; MAINTAIN; RELEASE;

D O I：

10.1016/j.stem.2017.11.003

中图分类号：

Q813 [细胞工程];

学科分类号：

100113 [医学细胞生物学];

摘要：

Myeloid-biased hematopoietic stem cells (MBHSCs) 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 H-2 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 H-2 agonist protects MB-HSCs from depletion after sepsis. Thus, histamine couples lineage-specific physiological demands to intrinsically primed MBHSCs to enforce homeostasis.

引用

页码：747 / +

页数：21

共 49 条

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