Soluble c-kit receptor mobilizes hematopoietic stem cells to peripheral blood in mice

Nakamura, Yuki; Tajima, Fumihito; Ishiga, Kiyomi; Yamazaki, Hidetoshi; Oshimura, Mitsuo; Shiota, Goshi; Murawaki, Yoshikazu

doi:10.1016/j.exphem.2004.01.004

Cited by 53 publications

(47 citation statements)

References 24 publications

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“…M uPAR also promotes adhesion of HSPCs to the BM microenvironment, as well as homing and engraftment of HSPCs, similar to α 4 β 1 and CXCR-4 (26,33,40,41). Our data also show that M uPAR is cleaved during mobilization of HSPCs, similar to cKit (42,43). We thus conclude that M uPAR is a receptor on HSPCs that regulates various processes of HSPCs in the BM.…”

Section: Discussionsupporting

confidence: 64%

Membrane-anchored uPAR regulates the proliferation, marrow pool size, engraftment, and mobilization of mouse hematopoietic stem/progenitor cells

et al. 2009

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The mechanisms of BM hematopoietic stem/progenitor cell (HSPC) adhesion, engraftment, and mobilization remain incompletely identified. Here, using WT and transgenic mice, we have shown that membrane-anchored plasminogen activator, urokinase receptor ( M uPAR) marks a subset of HSPCs and promotes the preservation of the size of this pool of cells in the BM. Loss or inhibition of M uPAR increased HSPC proliferation and impaired their homing, engraftment, and adhesion to the BM microenvironment. During mobilization, M uPAR was inactivated by plasmin via proteolytic cleavage. Cell-autonomous loss of the gene encoding M uPAR also impaired long-term engraftment and multilineage repopulation in primary and secondary recipient mice. These findings identify M uPAR and plasmin as regulators of the proliferation, marrow pool size, homing, engraftment, and mobilization of HSPCs and possibly also of HSCs.

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Section: Discussionsupporting

confidence: 64%

Membrane-anchored uPAR regulates the proliferation, marrow pool size, engraftment, and mobilization of mouse hematopoietic stem/progenitor cells

et al. 2009

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“…22 Moreover, disruption of c-kit signaling by the administration of soluble c-kit induces modest HPSC mobilization and also augments mobilization in response to G-CSF. 23 On the other hand, stimulation of c-kit signaling by administration of kitL induces robust HPSC mobilization 24 and c-kit-deficient mice have reduced G-CSF-induced mobilization. 25,26 In addition, mice deficient in the protease matrix metalloproteinase 9 (MMP-9), which is thought to mediate kitL cleavage, mobilize normally in most strains of mice.…”

Section: G-csf Mobilizes Hspcs Through a Hematopoietic Intermediatementioning

confidence: 99%

Mechanisms of G-CSF-mediated hematopoietic stem and progenitor mobilization

2010

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“…21,31,48 Data from a number of preclinical models showed that inhibition of these receptor-ligand interactions resulted in enhanced progenitor cell mobilization. [49][50][51] Although hematopoietic cells mobilized to peripheral blood for collection contain distinct populations of true stem cells and differentiated progenitor cells, they are often referred to collectively as stem cells. 52 In the BM and peripheral blood, stem cells are characterized by Ags specific to various lineages of hematopoietic cell differentiation.…”

Section: The Biology Of Stem Cell Mobilizationmentioning

confidence: 99%