Expression of GPI-80, a beta2-integrin-associated glycosylphosphatidylinositol-anchored protein, requires neutrophil differentiation with dimethyl sulfoxide in HL-60 cells.
GPI-80 is a member of the amidohydrolase family that has been proposed as a potential regulator of beta2-integrin-dependent leukocyte adhesion. GPI-80 is expressed mainly in human neutrophils. Our previous studies suggested that GPI-80 expression might be associated with myeloid differentiation. To verify this, we examined whether GPI-80 is expressed on the human promyelocytic leukemia cell line HL-60 following treatment with differentiation inducers. GPI-80 expression was induced in cells treated with dimethyl sulfoxide (DMSO) to stimulate differentiation down the neutrophil pathway. On the other hand, all-trans-retinoic acid (ATRA), another neutrophil-inducing reagent, induced no clear GPI-80 expression. Potent monocyte-inducing reagents such as 1alpha,25-dihydroxyvitamin D(3) or phorbol 12-myristate 13-acetate also had no significant effect on the protein expression. GPI-80-positive cells were found in the well-differentiated CD11b-positive and transferrin-receptor-negative cell population. Granulocyte colony-stimulating factor, which augments neutrophil differentiation of HL-60 cells, up-regulated GPI-80 expression in the presence of DMSO. Granulocyte/macrophage colony-stimulating factor, which is known to suppress the neutrophil maturation of cells, inhibited expression. Adhesion of DMSO-induced cells was regulated by anti-GPI-80 monoclonal antibody, similar to the regulation observed in neutrophils. These results suggest that use of DMSO to induce neutrophil differentiation provides suitable conditions for GPI-80 expression, and that this culture system may be a helpful model for further study of the regulation of GPI-80 expression during myeloid differentiation.
Department of Immunology and Parasitology, Yamagata University School of Medicine, Yamagata-City, 990-9585, Japan.
Yuji
Y
Takeda
Junfen
J
Fu
Kichiya
K
Suzuki
Dai
D
Sendo
Takeaki
T
Nitto
Fujiro
F
Sendo
Yoshihiko
Y
Araki
D000581:Amidohydrolases; D000906:Antibodies / Q000494:pharmacology; D018845:CD11 Antigens / Q000378:metabolism; D018821:CD18 Antigens / Q000235:genetics / Q000378:metabolism*; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000235:genetics*; D002762:Cholecalciferol / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D058851:GPI-Linked Proteins; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D018922:HL-60 Cells; D006801:Humans; D006867:Hydrolases; D008954:Models, Biological; D022423:Myeloid Cells / Q000187:drug effects / Q000378:metabolism*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D011990:Receptors, Transferrin / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology
D000906:Antibodies; D018845:CD11 Antigens; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D011990:Receptors, Transferrin; D016179:Granulocyte Colony-Stimulating Factor; D002762:Cholecalciferol; D014212:Tretinoin; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D006867:Hydrolases; D000581:Amidohydrolases; C121771:VNN2 protein, human; D013755:Tetradecanoylphorbol Acetate; D004121:Dimethyl Sulfoxide