Abstract
Granulocyte function may be altered after in vivo G-CSF administration and this has been related to both an immaturity of mobilized cells and to a defect in F-actin polymerization. In this paper we show that in resting Filgrastim (non-glycosylated G-CSF)-pulsed cells, F-actin polymerization, membrane-linked RhoA and cell polarization are enhanced compared to those found in resting Lenograstim (glycosylated G-CSF)-cells. The basal hyper-activation of RhoA could be responsible for the morphological and functional modifications of Filgrastim-mobilized cells. Moreover, Filgrastim-mobilized cells, but not Lenograstim-mobilized cells, are unable to correctly respond to LPS stimulation, as demonstrated by minor further RhoA activation and cell elongation.
MeSH terms
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Actins / chemistry
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Actins / drug effects
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Actins / physiology
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Cell Count
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Cell Polarity / drug effects
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Cell Polarity / physiology
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Filgrastim
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Glycosylation
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Granulocyte Colony-Stimulating Factor / chemistry
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Granulocyte Colony-Stimulating Factor / pharmacology*
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Granulocytes / cytology
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Granulocytes / drug effects*
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Granulocytes / physiology*
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Humans
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Lenograstim
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Lymphoma, Non-Hodgkin* / therapy
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Neutrophils / cytology
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Neutrophils / drug effects
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Neutrophils / physiology
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Peripheral Blood Stem Cell Transplantation
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Recombinant Proteins / pharmacology
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Remission Induction
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rhoA GTP-Binding Protein / metabolism
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rhoA GTP-Binding Protein / physiology*
Substances
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Actins
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Recombinant Proteins
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RHOA protein, human
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Granulocyte Colony-Stimulating Factor
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Lenograstim
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rhoA GTP-Binding Protein
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Filgrastim