Stromal‐derived factor 1 and matrix metalloproteinase 9 levels in bone marrow and peripheral blood of patients mobilized by granulocyte colony‐stimulating factor and chemotherapy. Relationship with mobilizing capacity of haematopoietic progenitor cells

Carion, Alexandra; Benboubker, Lotfi; Hérault, Olivier; Roingeard, Françoise; Degenne, Michel; Sénécal, Delphine; Desbois, Isabelle; Colombat, Philippe; Charbord, Pierre; Binet, Christian; Domenech, Jorge

doi:10.1046/j.1365-2141.2003.04545.x

Cited by 41 publications

(37 citation statements)

References 50 publications

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“…Furthermore, we also found that MMP inhibitor not only inhibited the SDF-1 degradation in BM, but also significantly decreased the number of WBC and CFC in the BALB/c mice PB. Although other data show that G-CSF-induced HSPC mobilization involves MMP-9, without reversing the positive gradient of SDF-1 between BM and PB, 34 our data suggested that disappearance of SDF-1 between BM and PB was related to the degrading activity of MMP-9, and MMP-9-dependent SDF-1-degradation might be a crucial step in HSPC mobilization.…”

Section: Discussionmentioning

confidence: 62%

Degradation of BM SDF-1 by MMP-9: the role in G-CSF-induced hematopoietic stem/progenitor cell mobilization

Jin

Zhai

Qiu

et al. 2008

Bone Marrow Transplant

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The major involvement of chemokines and proteolytic enzymes has recently been discovered in the mobilization process. Here, we report that the degradation of BM stromal cell-derived factor (SDF-1) by matrix metalloproteinase (MMP)-9 is important in G-CSF-mediated hematopoietic stem/progenitor cells (HSPCs) mobilization. In this study, the SDF-1 concentration in healthy donors BM plasma decreased significantly after 5 days of G-CSF administration, with no obvious change of SDF-1 in the peripheral blood. We also observed a similar result by immunohistochemical staining on the BM biopsy slides. In vitro, mobilized BM plasma exhibited decreased chemotactic effect on CD34 þ cells, compared with steady-state BM plasma. MMP-9 protein and mRNA increased dramatically in the BM plasma in accordance with SDF-1 decrease. MMP-9 enriched supernatant from HT1080 cell-conditioned medium upregulated CXCR4 expression and the migration of BM CD34 þ cells toward SDF-1. SDF-1 was a substrate for MMP-9, furthermore, SDF-1 also stimulated MMP-9 proteolytic enzyme activity of BM CD34 þ cells, which facilitate HSPCs migration. In BALB/c mice, HSPCs mobilization was significantly inhibited by anti-SDF-1 antibodies or MMP inhibitor, o-phenanthroline. In conclusion, the degradation of BM SDF-1 by MMP-9 is a vital step in mobilization.

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Section: Discussionmentioning

confidence: 62%

Degradation of BM SDF-1 by MMP-9: the role in G-CSF-induced hematopoietic stem/progenitor cell mobilization

Jin

Zhai

Qiu

et al. 2008

Bone Marrow Transplant

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“…We have recently reported that the uPAR-derived peptide uPAR 84-95 stimulates migration of human CD34 + KG1 cells and CD34 + HSCs, by activating fMLP receptors, and inactivates CXCR4, the chemokine receptor primarily responsible for HSC retention in bone marrow (6,(22)(23)(24)(25). We then investigated whether the same peptide is able to exert the same effects on mouse CD34 + M1 leukemia cells.…”

Section: Resultsmentioning

confidence: 99%

In vivo Activity of the Cleaved Form of Soluble Urokinase Receptor: A New Hematopoietic Stem/Progenitor Cell Mobilizer

et al. 2006

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Cleaved forms of soluble urokinase receptor (c-suPAR) have been detected in body fluids from patients affected by various tumors. We recently reported increased c-suPAR levels in sera of healthy donors during granulocyte colony-stimulating factor (G-CSF)-induced mobilization of CD34 + hematopoietic stem cells (HSC). In vitro, c-suPAR or its derived chemotactic peptide (uPAR [84][85][86][87][88][89][90][91][92][93][94][95] ) stimulated migration of human CD34 + HSCs and inactivated CXCR4, the chemokine receptor primarily responsible for HSC retention in bone marrow. These results suggested that c-suPAR could potentially contribute to regulate HSC trafficking from and to bone marrow. Therefore, we investigated uPAR 84-95 effects on mobilization of mouse CD34 + hematopoietic stem/progenitor cells (HSC/HPC). We first showed that uPAR 84-95 stimulated in vitro dose-dependent migration of mouse CD34 + M1 leukemia cells and inactivated murine CXCR4. uPAR [84][85][86][87][88][89][90][91][92][93][94][95] capability to induce mouse HSC/ HPC release from bone marrow and migration into the circulation was then investigated in vivo. uPAR 84-95 i.p. administration induced rapid leukocytosis, which was associated with an increase in peripheral blood CD34 + HSCs/HPCs. In vitro colony assays confirmed that uPAR 84-95 mobilized hematopoietic progenitors, showing an absolute increase in circulating colony-forming cells. uPAR [84][85][86][87][88][89][90][91][92][93][94][95] mobilizing activity was comparable to that of G-CSF; however, neither synergistic nor additive effect was observed in combining the two molecules. These findings show for the first time in vivo biological effects of c-suPAR. Its capability to mobilize HSCs suggests potential clinical applications in HSC transplantation. (Cancer Res 2006; 66(22): 10885-90)

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“…Indeed, we and others 13,25,26 have observed a negative correlation between the mobilization capacity and CXCR4 expression on CD34 þ cells. Our previous study demonstrated that the number of haematopoietic progenitors in the peripheral blood correlated with the percent of CXCR4-negative CD34 þ cells in the leukapheresis product.…”

Section: Discussionmentioning

confidence: 99%

The CXCL12-3′A allele is associated with a higher mobilization yield of CD34 progenitors to the peripheral blood of healthy donors for allogeneic transplantation

Bogunia‐Kubik

Gieryng

Dłubek

et al. 2009

Bone Marrow Transplant

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The interaction between CXCL12 and its receptor CXCR4 plays a crucial role in the homing and mobilization of haematopoietic progenitors. We investigated the putative association between a CXCL12 gene polymorphism, the G-A transition at position 801 in the 3 0 -untranslated region (3 0 UTR), and the yield of CD34 þ progenitors in 65 healthy allogeneic transplant donors who received G-CSF. Importantly, in this setting, the analysis was not biased by background disease or chemotherapy. The 3 0 UTR CXCL12 G801A polymorphism was detected using a PCR-RFLP technique with the MspI restriction enzyme and the frequency of CD34 þ progenitors was assessed by flow cytometry. The frequency as well as the number of CD34 þ progenitor cells in the first leukapheresis product was significantly higher from donors with the CXCL12-3 0 A allele compared to GG homozygotes (Po0.05 in both cases), especially for subjects with the CXCL12-3 0 AA homozygous genotype (Po0.01 in both cases). Moreover, more leukaphereses were needed to obtain the required number of CD34 þ progenitors for transplantation from CXCL12-3 0 GG homozygous donors compared to the CXCL12-3 0 A carriers (P ¼ 0.003). In conclusion, the CXCL12-3 0 A allele was associated with a higher yield of CD34 þ cells from healthy donors of PBPC for allogeneic haematopoietic SCT.

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Stromal‐derived factor 1 and matrix metalloproteinase 9 levels in bone marrow and peripheral blood of patients mobilized by granulocyte colony‐stimulating factor and chemotherapy. Relationship with mobilizing capacity of haematopoietic progenitor cells

Cited by 41 publications

References 50 publications

Degradation of BM SDF-1 by MMP-9: the role in G-CSF-induced hematopoietic stem/progenitor cell mobilization

Degradation of BM SDF-1 by MMP-9: the role in G-CSF-induced hematopoietic stem/progenitor cell mobilization

In vivo Activity of the Cleaved Form of Soluble Urokinase Receptor: A New Hematopoietic Stem/Progenitor Cell Mobilizer

The CXCL12-3′A allele is associated with a higher mobilization yield of CD34 progenitors to the peripheral blood of healthy donors for allogeneic transplantation

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