Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling

Chen, Weikai; Lv, Xin; Liu, Changlong; Chen, Ruoping; Liu, Jianhe; Dai, Huijuan; Zou, Gang‐Ming

doi:10.1002/jcp.25967

Cited by 9 publications

(8 citation statements)

References 32 publications

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“…The decrease in CD11b cells observed at d 1 in both groups might be due to immunosuppressive activity arising from the simultaneous increase in the levels of MSCs (50). The delayed increase in the BM CD11b + cells that occurred between d 1 and 7 postinjury might be a direct outcome of the increase in the percentage of HSCs that took place by d 3 and 7 and their consequent differentiation toward the myeloid lineage (51).…”

Section: Response Of Cd11b + Dendritic Cells and Macrophages To Inmentioning

confidence: 91%

Bone marrow cell response after injury and during early stage of regeneration is independent of the tissue‐of‐injury in 2 injury models

et al. 2018

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Selectively recruiting bone marrow (BM)-derived stem and progenitor cells to injury sites is a promising therapeutic approach. The coordinated action of soluble factors is thought to trigger the mobilization of stem cells from the BM and recruit them to lesions to contribute to tissue regeneration. Nevertheless, the temporal response profile of the major cellular players and soluble factors involved in priming the BM and recruiting BM-derived cells to promote regeneration is unknown. We show that injury alters the BM cellular composition, introducing population-specific fluctuations during tissue regeneration. We demonstrate that injury causes an immediate, transient response of mesenchymal stromal cells and endothelial cells followed by a nonoverlapping increase in hematopoietic stem and progenitor cells. Moreover, BM reaction is identical whether the injury is inflicted on skin and muscle or also involves a bone defect, but these 2 injury paradigms trigger distinct systemic cytokine responses. Together, our results indicate that the BM response to injury in the early stages of regeneration is independent of the tissue-of-injury based on the 2 models used, but the injured tissue dictates the systemic cytokine response.-Leitão, L., Alves, C. J., Alencastre, I. S., Sousa, D. M., Neto, E., Conceição, F., Leitão, C., Aguiar, P., Almeida-Porada, G., Lamghari, M. Bone marrow cell response after injury and during early stage of regeneration is independent of the tissue-of-injury in 2 injury models.

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Section: Response Of Cd11b + Dendritic Cells and Macrophages To Inmentioning

confidence: 91%

Bone marrow cell response after injury and during early stage of regeneration is independent of the tissue‐of‐injury in 2 injury models

et al. 2018

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“…LIGHT interacts with three different receptors (HVEM, LTβR, and decoy receptor 3), two of which are expressed on HSPCs 66 . HVEM signaling in murine HSPCs has been shown to induce myeloid differentiation in response to treatment with LIGHT in vitro and in vivo 66 . Here we show that signaling via LIGHT/ LTβR maintained the pool of HSCs and LSCs.…”

Section: Discussionmentioning

confidence: 99%

LIGHT/LTβR signaling regulates self-renewal and differentiation of hematopoietic and leukemia stem cells

et al. 2021

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The production of blood cells during steady-state and increased demand depends on the regulation of hematopoietic stem cell (HSC) self-renewal and differentiation. Similarly, the balance between self-renewal and differentiation of leukemia stem cells (LSCs) is crucial in the pathogenesis of leukemia. Here, we document that the TNF receptor superfamily member lymphotoxin-β receptor (LTβR) and its ligand LIGHT regulate quiescence and self-renewal of murine and human HSCs and LSCs. Cell-autonomous LIGHT/LTβR signaling on HSCs reduces cell cycling, promotes symmetric cell division and prevents primitive HSCs from exhaustion in serial re-transplantation experiments and genotoxic stress. LTβR deficiency reduces the numbers of LSCs and prolongs survival in a murine chronic myeloid leukemia (CML) model. Similarly, LIGHT/LTβR signaling in human G-CSF mobilized HSCs and human LSCs results in increased colony forming capacity in vitro. Thus, our results define LIGHT/LTβR signaling as an important pathway in the regulation of the self-renewal of HSCs and LSCs.

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“…Sca-1 is a marker specific to mouse HSCs and is used to identify and isolate HSCs 35 . C-kit is expressed on the surfaces of both early and differentiated HSCs/HCPs and helps the proliferation and differentiation of cells 36 . Experiments have found that sca-1 + HSC/HPC transplantation can reconstruct the hematopoietic function of non-obese diabetic/severe combined immunodeficient mice 36 .…”

Section: Discussionmentioning

confidence: 99%

“…C-kit is expressed on the surfaces of both early and differentiated HSCs/HCPs and helps the proliferation and differentiation of cells 36 . Experiments have found that sca-1 + HSC/HPC transplantation can reconstruct the hematopoietic function of non-obese diabetic/severe combined immunodeficient mice 36 . Encouragingly, SIPS significantly enhanced the proportion of HSCs/HPCs in the BMMNCs of mice with hematopoietic dysfunction, further confirming its role in improving hematopoietic function.…”

Section: Discussionmentioning

confidence: 99%

Sarcodon imbricatus polysaccharides improve mouse hematopoietic function after cyclophosphamide-induced damage via G-CSF mediated JAK2/STAT3 pathway

et al. 2018

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Sarcodon imbricatus, a rare medicinal and edible fungus, has various pharmacological bioactivities. We investigated the effects of S. imbricatus polysaccharides (SIPS) on hematopoietic function and identified the underlying mechanisms using in vitro experiments with CHRF, K562, and bone marrow mononuclear cells (BMMNCs) and in vivo experiments with a mouse model of cyclophosphamide-induced hematopoietic dysfunction. We found that SIPS induced proliferation and differentiation of CHRF and K562 cells and upregulated the expression of hematopoietic-related proteins, including p90 ribosomal S6 kinases (RSK1p90), c-Myc, and ETS transcription factor, in the two cell lines. After 28 days of treatment, SIPS enhanced the bodyweight and thymus indices of the mice, alleviated enlargement of the spleen and liver, and contributed to the recovery of peripheral blood to normal levels. More importantly, the percentages of B lymphocytes and hematopoietic stem cells or hematopoietic progenitor cells were significantly elevated in bone marrow. Based on an antibody chip analysis and enzyme-linked immunosorbent assay, SIPS were found to successfully regulate 12 cytokines to healthy levels in serum and spleen. The cytokines included the following: interleukins 1Ra, 2, 3, 4, 5, and 6, tumor necrosis factor α, interferon−γ, granulocyte colony-stimulating factor (G-CSF) and macrophage colony-stimulating factor (M-CSF), C-C motif chemokine1, and monocyte chemoattractant protein−1. Moreover, SIPS upregulated the phosphorylation levels of janus kinase 2 (JAK2) and the signal transducer and activator of transcription 3 (STAT3) in the spleen, and similar results were validated in CHRF cells, K562 cells, and BMMNCs. The data indicate that SIPS activated the JAK2/STAT3 pathway, possibly by interactions among multiple cytokines, particularly G-CSF. We found that SIPS was remarkably beneficial to the bone marrow hematopoietic system, and we anticipate that it could improve myelosuppression induced by long-term radiotherapy or chemotherapy.

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Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling

Cited by 9 publications

References 32 publications

Bone marrow cell response after injury and during early stage of regeneration is independent of the tissue‐of‐injury in 2 injury models

Bone marrow cell response after injury and during early stage of regeneration is independent of the tissue‐of‐injury in 2 injury models

LIGHT/LTβR signaling regulates self-renewal and differentiation of hematopoietic and leukemia stem cells

Sarcodon imbricatus polysaccharides improve mouse hematopoietic function after cyclophosphamide-induced damage via G-CSF mediated JAK2/STAT3 pathway

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