Neuronal regulation of bone marrow stem cell niches.
Neuronal regulation of bone marrow stem cell niches.
复制标题
骨髓干细胞龛的神经元调控。
DOI：
10.12688/f1000research.22554.1
复制
发表时间：
2020-01-01
期刊：
影响因子：
--
通讯作者：
Mendez-Ferrer, Simon
中科院分区：
文献类型：
--
作者：
Fielding, Claire;Mendez-Ferrer, Simon
骨髓是出生后造血和造血干细胞(HSC)维持的主要部位。骨髓间充质干细胞生态位是造血干细胞进化和响应生理需求的重要微环境。它负责协调造血干细胞的命运，并严格调控发生在骨髓中的过程，包括自我更新、静止、植入和谱系分化。然而，在血液应激后，如血液系统恶性肿瘤、电离辐射和化疗，骨髓HSC生态位受到干扰，导致细胞组成改变和重塑发生。因此，造血修复一直是许多研究的焦点，阐明这些机制具有重要的生物学和临床意义，即利用这些机制作为治疗恶性血液系统疾病的手段，促进骨髓损伤后的再生。交感神经系统在稳定状态下支配骨髓间充质的壁龛，调节造血干细胞的迁入和迁出。然而，最近的研究调查了交感神经和信号在应激状态下是如何失调的，以及它们对造血的后续影响。在这里，我们提供了不同的BM生态位的概述，以及它们如何有助于HSC的调节过程，特别是在稳态和应激造血下的神经元调节HSCs。
The bone marrow (BM) is the primary site of postnatal hematopoiesis and hematopoietic stem cell (HSC) maintenance. The BM HSC niche is an essential microenvironment which evolves and responds to the physiological demands of HSCs. It is responsible for orchestrating the fate of HSCs and tightly regulates the processes that occur in the BM, including self-renewal, quiescence, engraftment, and lineage differentiation. However, the BM HSC niche is disturbed following hematological stress such as hematological malignancies, ionizing radiation, and chemotherapy, causing the cellular composition to alter and remodeling to occur. Consequently, hematopoietic recovery has been the focus of many recent studies and elucidating these mechanisms has great biological and clinical relevance, namely to exploit these mechanisms as a therapeutic treatment for hematopoietic malignancies and improve regeneration following BM injury. The sympathetic nervous system innervates the BM niche andregulatesthe migration of HSCs in and out of the BM under steady state. However, recent studies have investigated how sympathetic innervation and signaling are dysregulated under stress and the subsequent effect they have on hematopoiesis. Here, we provide an overview of distinct BM niches and how they contribute to HSC regulatory processes with a particular focus on neuronal regulation of HSCs under steady state and stress hematopoiesis.