Augmented expression of platelet-activating factor receptor gene by TNF-alpha through transcriptional activation in human monocytes

Dagenais, P.; Thivierge, M.; Parent, J.L.; Stankova, J.; Rola-Pleszczynski, M.

Journal of Leukocyte Biology 61(1): 106-112

1997


ISSN/ISBN: 0741-5400
PMID: 9000543
DOI: 10.1002/jlb.61.1.106
Accession: 008203547

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Abstract
Tumor necrosis factor alpha (TNF-alpha) 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-alpha (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. [3H]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-alpha-pretreated monocytes. These observations provide new evidence for TNF-alpha and PAF interactions in human monocytes during inflammatory processes through up-regulation of PAFR expression by TNF-alpha.

Augmented expression of platelet-activating factor receptor gene by TNF-alpha through transcriptional activation in human monocytes