Abstract:
:Glucocorticoids, such as dexamethasone (Dex), are used clinically in the treatment of various inflammatory diseases. Dex acts by inhibiting the expression of inflammatory mediators, such as tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1). It is surprising that Dex enhances bacterial lipopolysaccharide (LPS) induction of tissue factor (TF) expression in human monocytic cells. TF is a transmembrane glycoprotein that activates the coagulation protease cascade. In this study, we analyze the mechanism by which Dex enhances LPS-induced TF expression in human monocytic cells. We found that Dex reduced LPS-induced TF gene transcription but increased the stability of TF mRNA. Dex decreased the stability of MCP-1 mRNA and did not affect TNF-alpha mRNA stability. Finally, we showed that Dex increased the stability of a transcript consisting of the final 297 nucleotides of the TF mRNA in in vitro decay assays. This region contains AU-rich elements that regulate mRNA stability and may mediate the Dex response. Therefore, despite an inhibition of TF gene transcription, Dex enhances TF expression in human monocytic cells by increasing the stability of TF mRNA.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Reddy KV,Bhattacharjee G,Schabbauer G,Hollis A,Kempf K,Tencati M,O'Connell M,Guha M,Mackman Ndoi
10.1189/jlb.0204068subject
Has Abstractpub_date
2004-07-01 00:00:00pages
145-51issue
1eissn
0741-5400issn
1938-3673pii
jlb.0204068journal_volume
76pub_type
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