title: Induction of Duffy gene (FY) in human endothelial cells and in mouse.
abstract: Duffy Blood Group protein is a glycoprotein with seven transmembrane domains that binds to C-X-C and C-C chemokines. The antigen is constitutively expressed in endothelial and epithelial cells of several nonerythroid tissues and in Purkinje cells of the cerebellum. We studied the effect of proinflammatory cytokines on Duffy gene expression in endothelial cells from human umbilical vein (HUVEC) and human pulmonary arteries (HPAEC). Also, we studied the effect of inflammatory agents like bacterial lipopolysaccharide (LPS) on Duffy gene induction in mouse. Reverse transcription-PCR and mRNA blot analyses showed that Duffy mRNA was present in these cells in negligible amounts. However, treatment with tumor necrosis factor-alpha for 6-24h resulted in a 5 to 8-fold increase in Duffy mRNA. On the other hand, treatment with interleukin-1 (IL-1), IL-6 or LPS did not have any effect. Fluorescence microscopy and fluorescence activated cell sorting showed greater expression of Duffy protein in treated cells correlating the increase in mRNA synthesis with an increase in antigen production. In mice, Duffy gene was induced in lungs and brain with LPS treatment indicating that the induction is a physiological event. Vascular endothelial cells may induce Duffy protein to regulate leukocytes and/or chemokine trafficking.
authors.affiliation: Laboratory of Cell Biology, The New York Blood Center, 310 East 67th Street, New York, NY 10021, USA. asok_chaudhuri@nybc.org
authors.forename: Asok
authors.initials: A
authors.lastname: Chaudhuri
authors.forename: Marilis
authors.initials: M
authors.lastname: Rodriguez
authors.forename: Valerie
authors.initials: V
authors.lastname: Zbrzezna
authors.forename: Hong
authors.initials: H
authors.lastname: Luo
authors.forename: A Oscar
authors.initials: AO
authors.lastname: Pogo
authors.forename: Deben
authors.initials: D
authors.lastname: Banerjee
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002469:Cell Separation; D002478:Cells, Cultured; D054426:Chemokine CXCL2; D003513:Cycloheximide / Q000494:pharmacology; D004375:Duffy Blood-Group System / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008856:Microscopy, Fluorescence; D015846:Monokines / Q000096:biosynthesis; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011651:Pulmonary Artery / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014471:Umbilical Veins / Q000378:metabolism*
chemical_list: C473745:ACKR1 protein, human; D054426:Chemokine CXCL2; D004375:Duffy Blood-Group System; D008070:Lipopolysaccharides; D015846:Monokines; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha; D003513:Cycloheximide