Hematopoiesis produce every day billions of blood cells and takes place in the bone marrow (BM) by the proliferation and differentiation of hematopoietic stem cells (HSC). HSC are found mainly adjacent to the BM vascular sinusoids where endothelial cells and mesenchimal stromal cells promote HSC maintenance by producing a variety of factors. Other cell types that regulate HSC niches include sympathetic nerves, non–myelinating Schwann cells and a variety of mature hematopoietic cells such as macrophages, neutrophils, and megakaryocytes. This review will focus on the role of adrenergic signals, i.e. of catecholamines, in the regulation of the HSC niche. The available evidence is rather controversial possibly due to the fact that adrenergic receptors are expressed by many cellular components of the niche and also by the often neglected observation that catecholamines may be produced and released also by the BM cells themselves. In addition one has to consider that, physiologically, the sympathetic nervous system (SNS) activity follows a circadian rhythmicity as driven by the suprachiasmatic nucleus (SCN) of the hypothalamus but may be also activated by cognitive and non-cognitive environmental stimuli. The adrenergic modulation of hematopoiesis holds a considerable potential for pharmacological therapeutic approaches in a variety of hematopoietic disorders and for HSC transplantation however the complexity of the system demands further studies.

Sympathetic nerve termini may release NE while mature BM cells may release norepinephrine (NE) and / or epinephrine (E). Both may bind to β-adrenergic receptor (AR) expressed in nestin+MSC in the hematopoietic stem cell (HSC) niche and regulate the physiological trafficking of HSC by modulating the expression of CXCL12 and SCF. Both NE and E may also activate Lin − c-Kit+ Sca-1+ (LKS) cell via another AR. In addition, NE may also signal to α1-AR expressed in pre-B cells which by TGF-β secretion might regulate proliferation of their lymphoid progenitors in an autocrine manner and/or inhibit myeloid progenitors

中文翻译：

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造血的肾上腺素调节。

造血活动每天产生数十亿个血细胞，并通过造血干细胞（HSC）的增殖和分化在骨髓（BM）中发生。发现HSC主要靠近BM血管正弦曲线，其中内皮细胞和间质基质细胞通过产生多种因素促进HSC维持。调节HSC壁ni的其他细胞类型包括交感神经，无髓鞘的雪旺细胞和各种成熟的造血细胞，例如巨噬细胞，嗜中性粒细胞和巨核细胞。本文将重点探讨肾上腺素能信号（即儿茶酚胺）在调节HSC利基中的作用。可用的证据颇具争议，可能是由于肾上腺素能受体由利基的许多细胞成分表达，而且由于经常被忽视的观察结果表明，儿茶酚胺也可能由BM细胞自身产生和释放而引起争议。另外，必须考虑到，在生理上，交感神经系统（SNS）的活动遵循由下丘脑的视交叉上核（SCN）驱动的昼夜节律，但也可能由认知和非认知环境刺激激活。造血功能的肾上腺素调节对于各种造血疾病和HSC移植的药理学治疗方法具有相当大的潜力，但是该系统的复杂性需要进一步研究。交感神经系统（SNS）的活动遵循由下丘脑的上视交叉核（SCN）驱动的昼夜节律，但也可能由认知和非认知环境刺激激活。造血功能的肾上腺素调节对于各种造血疾病和HSC移植的药理学治疗方法具有相当大的潜力，但是该系统的复杂性需要进一步研究。交感神经系统（SNS）的活动遵循由下丘脑的上视交叉核（SCN）驱动的昼夜节律，但也可能由认知和非认知环境刺激激活。造血功能的肾上腺素调节对于各种造血疾病和HSC移植的药理学治疗方法具有相当大的潜力，但是该系统的复杂性需要进一步研究。

交感神经末端可能释放NE，而成熟的BM细胞则可能释放去甲肾上腺素（NE）和/或肾上腺素（E）。两者都可能与造血干细胞（HSC）巢中Nestin + MSC中表达的β-肾上腺素受体（AR）结合，并通过调节CXCL12和SCF的表达来调节HSC的生理运输。NE和E还可通过另一个AR激活Lin-c-Kit + Sca-1 +（LKS）细胞。此外，NE还可能向前B细胞中表达的α1-AR发出信号，该信号通过TGF-β的分泌可能以自分泌方式调节其淋巴祖细胞的增殖和/或抑制骨髓祖细胞。