Bone marrow sinusoidal endothelium as a facilitator/regulator of cell egress from the bone marrow

Hassanshahi, Mohammadhossein; Hassanshahi, Alireza; Khabbazi, Samira; Su, Yu Wen; Chen, Xian

doi:10.1016/j.critrevonc.2019.01.024

Cited by 17 publications

(11 citation statements)

References 195 publications

(185 reference statements)

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“…Lactate increases BM endothelium permeability via GPR81. Others and we have shown that BM sinusoidal vessels are more permeable and serve as the exclusive trafficking site for both immature hematopoietic stem cells and mature leukocytes 24,[34][35][36] . To assess the involvement of BM sinusoidal "leakiness" in LPS-and lactate-induced neutrophil mobilization, we measured the penetration of Evans Blue Dye (EBD) from the circulation into the BM, a classical readout of BM vascular permeability.…”

Section: Resultsmentioning

confidence: 78%

Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling

et al. 2020

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Neutrophils provide first line of host defense against bacterial infections utilizing glycolysis for their effector functions. How glycolysis and its major byproduct lactate are triggered in bone marrow (BM) neutrophils and their contribution to neutrophil mobilization in acute inflammation is not clear. Here we report that bacterial lipopolysaccharides (LPS) or Salmonella Typhimurium triggers lactate release by increasing glycolysis, NADPH-oxidasemediated reactive oxygen species and HIF-1α levels in BM neutrophils. Increased release of BM lactate preferentially promotes neutrophil mobilization by reducing endothelial VE-Cadherin expression, increasing BM vascular permeability via endothelial lactate-receptor GPR81 signaling. GPR81 −/− mice mobilize reduced levels of neutrophils in response to LPS, unless rescued by VE-Cadherin disrupting antibodies. Lactate administration also induces release of the BM neutrophil mobilizers G-CSF, CXCL1 and CXCL2, indicating that this metabolite drives neutrophil mobilization via multiple pathways. Our study reveals a metabolic crosstalk between lactate-producing neutrophils and BM endothelium, which controls neutrophil mobilization under bacterial infection.

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Section: Resultsmentioning

confidence: 78%

Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling

et al. 2020

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“…The term stem cell mobilization is usually used to refer to induced mechanisms of cell egress from the marrow. Marrow sinusoidal endothelium is a regulator of cell egress from the marrow just as it is important for homing 68 . Marrow cell mobilization into the peripheral blood takes place in regions where the adventitial cells are absent, and the barrier is just the sinusoidal endothelium.…”

Section: Stem Cell Mobilizationmentioning

confidence: 99%

Stem cell homing: From physiology to therapeutics

2020

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Stem cell homing is a multistep endogenous physiologic process that is also used by exogenously administered hematopoietic stem and progenitor cells (HSPCs). This multistep process involves cell migration and is essential for hematopoietic stem cell transplantation. The process can be manipulated to enhance ultimate engraftment potential, and understanding stem cell homing is also important to the understanding of stem cell mobilization. Homing is also of potential importance in the recruitment of marrow mesenchymal stem and stromal cells (MSCs) to sites of injury and regeneration. This process is less understood but assumes importance when these cells are used for repair purposes. In this review, the process of HSPC and MSC homing is examined, as are methods to enhance this process.

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“…In contrast, ~40% of ILC2P were assigned to the sinusoidal niche. These data indicate that ILC progenitor populations are heterogeneous in their localization within the BM, and the majority of the multipotential ILCPs are present in the sinusoid niche, which is considered not only a major site of hematopoiesis but also the gate for cell trafficking in and out of the BM ( 32 ). To determine whether these BM ILC progenitors emigrate to the peripheral blood, we took a BM CellTracker microinjection approach ( 33 ).…”

Section: Resultsmentioning

confidence: 99%

Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors

et al. 2022

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Innate lymphoid cells (ILCs) play crucial roles in maintenance and defense of peripheral tissues but would undergo natural and inflammation-induced attrition over time. A potential solution to counteract the peripheral ILC attrition would be regulated mobilization of bone marrow (BM) ILC progenitors. The major multipotential ILC progenitors (ILCPs) are divided into two subsets in distinct niches of the BM. Sinusoid ILCPs emigrate from the BM to circulate the peripheral blood. In contrast, parenchyma ILCPs are more likely in cell cycling and less likely to emigrate BM. The mobilization of BM ILCPs is internally and externally controlled by the coordinated expression of the BM retention receptors (Itg-α4 and CXCR4) and the emigration receptors sphingosine-1-phosphate (S1P) receptors. The expression of the BM retention and emigration receptors is developmentally regulated in the steady state and by the inflammasome-derived IL-18. Upon infusion, sinusoid ILCPs can effectively restore peripheral ILC insufficiency and tissue integrity during inflammatory responses.

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Bone marrow sinusoidal endothelium as a facilitator/regulator of cell egress from the bone marrow

Cited by 17 publications

References 195 publications

Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling

Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling

Stem cell homing: From physiology to therapeutics

Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors

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