CD26 is essential for normal G-CSF-induced progenitor cell mobilization as determined by CD26-/- mice

Kent W. Christopherson, Scott Cooper, Giao Hangoc, Hal Broxmeyer

Research output: Contribution to journalArticle

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Abstract

Objective. In spite of the wide usage of mobilized peripheral blood hematopoietic stem and progenitor cells (HSC/HPC) for transplantation, the mechanism of granulocyte colony-stimulating factor (G-CSF)-induced HSC/HPC mobilization has yet to be fully determined. Our previous studies suggested that that G-CSF-induced mobilization may involve the extracellular peptidase CD26 (DPPIV/dipeptidylpeptidase IV). We set out to establish whether CD26 was an essential component of normal G-CSF-induced mobilization of HSC/HPC. Materials and methods. Normal wild-type (WT) control C57BL/6 mice and CD26 knockout (CD26-/-) mice, also on a C57BL/6 background, were treated with or without G-CSF and peripheral blood cells, bone marrow cells, and spleen cells were assessed for CFU-GM, BFU-E, and CFU-GEMM content. Results. No statistical difference in the number of CFU-GM, BFU-E, or CFU-GEMM in the peripheral blood, bone marrow, or spleen of untreated WT vs untreated CD26 -/- mice was observed. G-CSF treatment of WT mice resulted in the mobilization of HPC into the peripheral blood. The number of HPC detected in G-CSF-treated CD26-/- mouse peripheral blood was significantly less than the corresponding number of HPC detected in G-CSF-treated WT mouse peripheral blood after either a 2- or 4-day G-CSF regimen. Conclusions. CD26 plays a critical role in G-CSF-induced mobilization of HPC.

Original languageEnglish
Pages (from-to)1126-1134
Number of pages9
JournalExperimental Hematology
Volume31
Issue number11
DOIs
StatePublished - Nov 2003

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Granulocyte Colony-Stimulating Factor
Stem Cells
Myeloid Progenitor Cells
Granulocyte-Macrophage Progenitor Cells
Erythroid Precursor Cells
Hematopoietic Stem Cells
Spleen
Inbred C57BL Mouse
Knockout Mice
Bone Marrow Cells
Blood Cells
Peptide Hydrolases
Transplantation
Bone Marrow

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Genetics
  • Hematology
  • Oncology
  • Transplantation

Cite this

CD26 is essential for normal G-CSF-induced progenitor cell mobilization as determined by CD26-/- mice. / Christopherson, Kent W.; Cooper, Scott; Hangoc, Giao; Broxmeyer, Hal.

In: Experimental Hematology, Vol. 31, No. 11, 11.2003, p. 1126-1134.

Research output: Contribution to journalArticle

Christopherson, Kent W. ; Cooper, Scott ; Hangoc, Giao ; Broxmeyer, Hal. / CD26 is essential for normal G-CSF-induced progenitor cell mobilization as determined by CD26-/- mice. In: Experimental Hematology. 2003 ; Vol. 31, No. 11. pp. 1126-1134.
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abstract = "Objective. In spite of the wide usage of mobilized peripheral blood hematopoietic stem and progenitor cells (HSC/HPC) for transplantation, the mechanism of granulocyte colony-stimulating factor (G-CSF)-induced HSC/HPC mobilization has yet to be fully determined. Our previous studies suggested that that G-CSF-induced mobilization may involve the extracellular peptidase CD26 (DPPIV/dipeptidylpeptidase IV). We set out to establish whether CD26 was an essential component of normal G-CSF-induced mobilization of HSC/HPC. Materials and methods. Normal wild-type (WT) control C57BL/6 mice and CD26 knockout (CD26-/-) mice, also on a C57BL/6 background, were treated with or without G-CSF and peripheral blood cells, bone marrow cells, and spleen cells were assessed for CFU-GM, BFU-E, and CFU-GEMM content. Results. No statistical difference in the number of CFU-GM, BFU-E, or CFU-GEMM in the peripheral blood, bone marrow, or spleen of untreated WT vs untreated CD26 -/- mice was observed. G-CSF treatment of WT mice resulted in the mobilization of HPC into the peripheral blood. The number of HPC detected in G-CSF-treated CD26-/- mouse peripheral blood was significantly less than the corresponding number of HPC detected in G-CSF-treated WT mouse peripheral blood after either a 2- or 4-day G-CSF regimen. Conclusions. CD26 plays a critical role in G-CSF-induced mobilization of HPC.",
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N2 - Objective. In spite of the wide usage of mobilized peripheral blood hematopoietic stem and progenitor cells (HSC/HPC) for transplantation, the mechanism of granulocyte colony-stimulating factor (G-CSF)-induced HSC/HPC mobilization has yet to be fully determined. Our previous studies suggested that that G-CSF-induced mobilization may involve the extracellular peptidase CD26 (DPPIV/dipeptidylpeptidase IV). We set out to establish whether CD26 was an essential component of normal G-CSF-induced mobilization of HSC/HPC. Materials and methods. Normal wild-type (WT) control C57BL/6 mice and CD26 knockout (CD26-/-) mice, also on a C57BL/6 background, were treated with or without G-CSF and peripheral blood cells, bone marrow cells, and spleen cells were assessed for CFU-GM, BFU-E, and CFU-GEMM content. Results. No statistical difference in the number of CFU-GM, BFU-E, or CFU-GEMM in the peripheral blood, bone marrow, or spleen of untreated WT vs untreated CD26 -/- mice was observed. G-CSF treatment of WT mice resulted in the mobilization of HPC into the peripheral blood. The number of HPC detected in G-CSF-treated CD26-/- mouse peripheral blood was significantly less than the corresponding number of HPC detected in G-CSF-treated WT mouse peripheral blood after either a 2- or 4-day G-CSF regimen. Conclusions. CD26 plays a critical role in G-CSF-induced mobilization of HPC.

AB - Objective. In spite of the wide usage of mobilized peripheral blood hematopoietic stem and progenitor cells (HSC/HPC) for transplantation, the mechanism of granulocyte colony-stimulating factor (G-CSF)-induced HSC/HPC mobilization has yet to be fully determined. Our previous studies suggested that that G-CSF-induced mobilization may involve the extracellular peptidase CD26 (DPPIV/dipeptidylpeptidase IV). We set out to establish whether CD26 was an essential component of normal G-CSF-induced mobilization of HSC/HPC. Materials and methods. Normal wild-type (WT) control C57BL/6 mice and CD26 knockout (CD26-/-) mice, also on a C57BL/6 background, were treated with or without G-CSF and peripheral blood cells, bone marrow cells, and spleen cells were assessed for CFU-GM, BFU-E, and CFU-GEMM content. Results. No statistical difference in the number of CFU-GM, BFU-E, or CFU-GEMM in the peripheral blood, bone marrow, or spleen of untreated WT vs untreated CD26 -/- mice was observed. G-CSF treatment of WT mice resulted in the mobilization of HPC into the peripheral blood. The number of HPC detected in G-CSF-treated CD26-/- mouse peripheral blood was significantly less than the corresponding number of HPC detected in G-CSF-treated WT mouse peripheral blood after either a 2- or 4-day G-CSF regimen. Conclusions. CD26 plays a critical role in G-CSF-induced mobilization of HPC.

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