title: Switch of histamine receptor expression from H2 to H1 during differentiation of monocytes into macrophages.
abstract: It is known that histamine suppresses gene expression and synthesis of tumor necrosis factor alpha (TNF-alpha) induced by lipopolysaccharide (LPS) in human peripheral blood mononuclear monocytes (HPM) or alveolar macrophages via histamine H2 receptors. We investigated the effect of histamine and differentiation in macrophages on the expression and secretion of TNF-alpha, TNF-alpha-converting enzyme (TACE), and histamine H1 and H2 receptors by use of a leukemia cell line, U937, and HPM. Differentiation of U937 and HPM cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced the H1 receptor expression and rather suppressed the H2 receptor, resulting in up-regulation of the histamine-induced expression and secretion of TNF-alpha, modulated via TACE. Therefore, histamine failed to inhibit up-regulated expression of TNF-alpha induced by LPS in macrophages. The switch from H2 to H1 receptors during differentiation in the monocyte/macrophage lineage could participate in the pathogenic processes of atherosclerosis and inflammatory reactions in the arterial wall.
authors.affiliation: Department of Pathology and Cell Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
authors.forename: K Y
authors.initials: KY
authors.lastname: Wang
authors.forename: N
authors.initials: N
authors.lastname: Arima
authors.forename: S
authors.initials: S
authors.lastname: Higuchi
authors.forename: S
authors.initials: S
authors.lastname: Shimajiri
authors.forename: A
authors.initials: A
authors.lastname: Tanimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Murata
authors.forename: T
authors.initials: T
authors.lastname: Hamada
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaguri
mesh_terms: D051722:ADAM Proteins; D000072198:ADAM17 Protein; D015152:Blotting, Northern; D002454:Cell Differentiation; D002478:Cells, Cultured; D002927:Cimetidine / Q000494:pharmacology; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000166:cytology* / Q000378:metabolism; D008666:Metalloendopeptidases / Q000378:metabolism; D009000:Monocytes / Q000166:cytology* / Q000378:metabolism; D011969:Receptors, Histamine H1 / Q000378:metabolism*; D011970:Receptors, Histamine H2 / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D020298:U937 Cells; D015854:Up-Regulation
chemical_list: D006635:Histamine H2 Antagonists; D008070:Lipopolysaccharides; D011969:Receptors, Histamine H1; D011970:Receptors, Histamine H2; D014409:Tumor Necrosis Factor-alpha; D002927:Cimetidine; D051722:ADAM Proteins; D008666:Metalloendopeptidases; D000072198:ADAM17 Protein; C000606462:ADAM17 protein, human; D013755:Tetradecanoylphorbol Acetate