title: Suppression of CXCR4 expression in mast cells upon IgE-mediated antigen stimulation.
abstract: OBJECTIVE
  Recent studies have demonstrated that a variety of chemokine receptors are expressed in mast cells. We investigated the changes in mRNA expression of CXCRs in murine IL-3-dependent bone marrow-derived mast cells (BMMCs) to clarify how the CXCR expression is regulated in mast cells.
  
  
  METHODS
  Expression of CXCR mRNA was measured by RNase protection assay. Functional expression of CXCRs was confirmed by monitoring intracellular Ca(2+) mobilization.
  
  
  RESULTS
  CXCR4 mRNA expression was transiently induced in BMMCs in serum-dependent fashion and was completely suppressed upon IgE-mediated antigen stimulation. In contrast, CXCR5 mRNA expression was induced upon IgE-mediated antigen stimulation. Changes in the intracellular Ca(2+) mobilization induced by CXCL12 strongly indicated the functional expression of CXCR4. The decrease in CXCR4 and the increase in CXCR5 mRNA expression was also observed in BMMCs stimulated with thapsigargin, a phorbol ester, and stem cell factor.
  
  
  CONCLUSIONS
  The mRNA expression of CXCR4 is differentially regulated in BMMCs upon various stimuli including IgE-mediated antigen stimulation.
authors.affiliation: Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
authors.forename: Junji
authors.initials: J
authors.lastname: Matsuura
authors.forename: Mariko
authors.initials: M
authors.lastname: Sakanaka
authors.forename: Norio
authors.initials: N
authors.lastname: Sato
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ichikawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism*; D001854:Bone Marrow Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D007073:Immunoglobulin E / Q000378:metabolism*; D007377:Interleukin-3 / Q000378:metabolism; D008407:Mast Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D010703:Phorbol Esters / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism*; D054380:Receptors, CXCR5 / Q000378:metabolism; D019089:Stem Cell Factor / Q000494:pharmacology; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D000941:Antigens; C514936:CXCR4 protein, mouse; C513179:CXCR5 protein, mouse; D004791:Enzyme Inhibitors; D007377:Interleukin-3; D010703:Phorbol Esters; D012333:RNA, Messenger; D019718:Receptors, CXCR4; D054380:Receptors, CXCR5; D019089:Stem Cell Factor; D007073:Immunoglobulin E; D000001:Calcimycin; D019284:Thapsigargin; D002118:Calcium
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