Abstract
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 and regulates the 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.
Highlights
The bone marrow (BM) is the primary site of postnatal hematopoiesis and hematopoietic stem cell (HSC) maintenance
Stromal cells can be further divided to neuron-glial antigen (NG2)-expressing cells[2], Cxcl12-abundant reticular (CAR) cells[7], and cells expressing leptin receptor (LepR)[1], all of which overlap with Nestin-green fluorescent protein (Nes-GFP)+ cells to varying degrees[8,9]
Conclusions and future perspectives The BM is regulated by neural signals principally emerging from the autonomic nervous system
Summary
Faculty Reviews are written by members of the prestigious Faculty Opinions Faculty. They are commissioned and are peer reviewed before publication to ensure that the final, published version is comprehensive and accessible. Cardiovascular disease Ischemic myocardium causes the heart to initiate the influx of circulating myeloid cells to the site of damage This results in the SNS signaling to the BM to increase the production of leukocytes to meet the demand, aided by circulating mediators such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-1β produced by the heart[58,59,60,61]. These effects were reversed with the treatment of propranolol, which is a non-selective beta blocker[63,64] Following on from those studies and previous studies on adrenergic HSC regulation[35], chronic psychosocial stress was demonstrated to act on the most primitive progenitors, causing an increase in the proliferation of HSPCs in the BM of mice[65]. ↑ Pro-inflammatory genes (e.g., interleukin 1 beta [IL1B], tumor necrosis factor, and IL-8)
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