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Augmented expression of platelet‐activating factor receptor gene by TNF‐α through transcriptional activation in human monocytes
Author(s) -
Dagenais Pierre,
Thivierge Maryse,
Parent JeanLuc,
Stankova Jana,
RolaPleszczynski Marek
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.61.1.106
Subject(s) - tumor necrosis factor alpha , platelet activating factor receptor , biology , platelet activating factor , monocyte , cytokine , receptor , microbiology and biotechnology , tissue factor , gene expression , messenger rna , pathogenesis , immunology , medicine , gene , biochemistry , antagonist , coagulation
Tumor necrosis factor α (TNF‐α) is a cytokine produced by activated monocytes and often associated with platelet‐activating factor (PAF) during the pathogenesis of many inflammatory and infectious diseases. PAFR is a G‐protein‐coupled receptor constitutively expressed on monocytes. TNF‐α (100–400 U/mL) significantly increased PAFR mRNA expression in human monocytes. This increase was seen after 1 h of stimulation and persisted up to 24 h. Actinomycin D pretreatment studies revealed a transcriptional increase in PAFR gene expression without effect on mRNA half‐life. [ 3 H]WEB 2086 binding studies showed a significant (43%) increase in specific binding sites in 24‐h‐treated cells without change in receptor affinity. Increased interleukin‐6 production in response to PAF was also found in 24‐h TNF‐α‐pretreated monocytes. These observations provide new evidence for TNF‐α and PAF interactions in human monocytes during inflammatory processes through up‐regulation of PAFR expression by TNF‐α. J. Leukoc. Biol . 61: 106–112; 1997.