Reciprocal effects of pro-inflammatory stimuli and anti-inflammatory drugs on the activity of heat shock factor-1 in human monocytes.
Heat shock factor-1 (HSF-1), the transcriptional activator of heat shock genes has recently been shown to play a role in the repression of acute phase genes. We have further explored the role of HSF-1 in inflammatory processes in human monocytes. HSF-1 was activated in these cells by a wide range of classes of non-steroidal antiinflammatory drugs (NSAIDs) while being strongly repressed by pro-inflammatory stimuli. The experiments indicate reciprocal regulation of the acute phase and heat shock responses and suggest a novel target for the NSAID family of drugs.
Soncin
F
F
Dana Farber Cancer Institute, Boston, Massachusetts, USA.
Calderwood
S K
SK
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002460:Cell Line; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004268:DNA-Binding Proteins / Q000378:metabolism*; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D006893:Hydroxyeicosatetraenoic Acids / Q000378:metabolism; D018836:Inflammation Mediators; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D014157:Transcription Factors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins; D006893:Hydroxyeicosatetraenoic Acids; D018836:Inflammation Mediators; D014157:Transcription Factors