Positioning of bone marrow hematopoietic and stromal cells relative to blood flow in vivo: serially reconstituting hematopoietic stem cells reside in distinct nonperfused niches

Winkler, Ingrid G.; Barbier, Valérie; Wadley, Robert; Zannettino, Andrew C.W.; Williams, Sharon A.; Lévesque, Jean‐Pierre

doi:10.1182/blood-2009-07-233437

Cited by 216 publications

(209 citation statements)

References 45 publications

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“…Recent studies have identified some essential cellular components of the HSC niche in the murine bone marrow, including osteoblasts (Calvi et al, 2003;Zhang et al, 2003;Arai et al, 2004), sinusoidal endothelial cells (Kiel et al, 2005), mesenchymal stem cells (MSCs) (Mendez-Ferrer et al, 2010;Kunisaki et al, 2013), perivascular cells (Sugiyama et al, 2006), macrophages (Winkler et al, 2010), and megakaryocytes (Zhao et al, 2014;Bruns et al, 2014;Nakamura-Ishizu et al, 2014).…”

Section: The Hsc Niche In the Teleost Kidneymentioning

confidence: 99%

Isolation and characterization of hematopoietic stem cells in teleost fish

Kobayashi

Katakura

Moritomo

2016

Developmental & Comparative Immunology

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Despite 400 million years of evolutionary divergence, hematopoiesis is highly conserved between mammals and teleost fish. All types of mature blood cells including the erythroid, myeloid, and lymphoid lineages show a high degree of similarity to their mammalian counterparts at the morphological and molecular level. Hematopoietic stem cells (HSCs) are cells that are capable of self-renewal and differentiating into all hematopoietic lineages over the lifetime of an organism. The study of HSCs has been facilitated through bone marrow transplantation experiments developed in the mouse model. In the last decade, the zebrafish and clonal ginbuna carp (Carassius auratus langsdorfii) have emerged as new models for the study of HSCs. This review highlights the recent progress and future prospects of studying HSCs in teleost fish.Transplantation assays using these teleost models have demonstrated the presence of HSCs in the kidney, which is the major hematopoietic organ in teleost fish. Moreover, it is possible to purify HSCs from the kidney utilizing fluorescent dyes or transgenic animals. These teleost models will provide novel insights into the universal mechanisms of HSC maintenance, homeostasis, and differentiation among vertebrates.

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Section: The Hsc Niche In the Teleost Kidneymentioning

confidence: 99%

Isolation and characterization of hematopoietic stem cells in teleost fish

Kobayashi

Katakura

Moritomo

2016

Developmental & Comparative Immunology

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“…PDGFRa + CD51 + MSC [36] and PDGFRa + Sca1 + MSC [37] were detected using methods and reagents as described by Winkler et al [38], Schepers et al [39], Morikawa et al [37], Houlihan et al [40] and Pinho et al [36]. Femurs, tibias, humeri, ulnas, radii, and pelvis were dissected.…”

Section: In Vivo Msc Immunophenotyping By Flow Cytometrymentioning

confidence: 99%

SHIP1 Regulates MSC Numbers and Their Osteolineage Commitment by Limiting Induction of the PI3K/Akt/β-Catenin/Id2 Axis

Iyer

Viernes

Chisholm³

et al. 2014

Stem Cells and Development

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Here, we show that Src homology 2-domain-containing inositol 5¢-phosphatase 1 (SHIP1) is required for the efficient development of osteoblasts from mesenchymal stem cells (MSCs) such that bone growth and density are reduced in mice that lack SHIP1 expression in MSCs. We find that SHIP1 promotes the osteogenic output of MSCs by limiting activation of the PI3K/Akt/b-catenin pathway required for induction of the MSC stemness factor Id2. In parallel, we demonstrate that mice with myeloid-restricted ablation of SHIP1, including osteoclasts (OCs), show no reduction in bone mass or density. Hence, diminished bone mass and density in the SHIP1-deficient mice results from SHIP deficiency in MSC and osteolineage progenitors. Intriguingly, mice with a SHIP-deficient MSC compartment also exhibit decreased OC numbers. In agreement with our genetic findings we also show that treatment of mice with an SHIP1 inhibitor (SHIPi) significantly reduces bone mass. These findings demonstrate a novel role for SHIP1 in MSC fate determination and bone growth. Further, SHIPi may represent a novel therapeutic approach to limit bone development in osteopetrotic and sclerotic bone diseases.

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“…The in vivo effects of G-CSF on EC are also influenced by the involvement of infiltrated neutrophils and their secreted proangiogenic cytokines such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), which leads to neovascularisation [80,81] and dissociation of tight junction element vascular endothelial cadherin (VE-cad) [82,83]. However, it must be noted that G-CSF treatment does not lead to measurable vascular leakage as determined by Evans Blue perfusion [84]. This is in contrast with CYP treatment, which disrupts the continuity of BM vascular beds [15,85] and dramatically increases vascular leakage in the BM [84].…”

Section: Endothelial Cells (Ecs)mentioning

confidence: 99%

“…However, it must be noted that G-CSF treatment does not lead to measurable vascular leakage as determined by Evans Blue perfusion [84]. This is in contrast with CYP treatment, which disrupts the continuity of BM vascular beds [15,85] and dramatically increases vascular leakage in the BM [84]. The fact that cyclophosphamide causes vascular leakage in the BM while G-CSF does not may explain in part why cyclophosphamide is a more potent mobilizer than G-CSF, and that these two agents synergize together.…”

Section: Endothelial Cells (Ecs)mentioning

confidence: 99%