title: Heat shock treatment suppresses angiotensin II-induced SP-1 and AP-1 and stimulates Oct-1 DNA-binding activity in heart.
abstract: OBJECTIVE
  Heat shock (HS) treatment (42 degrees C for 15 min) and the expression of heat shock proteins (Hsps) protect against angiotensin (Ang) II-induced inflammation in aorta and heart by suppressing the activation of the pro-inflammatory transcription factor NF-kappaB. In this study we examined pro-inflammatory transcription factors SP-1, AP-1 and an anti-inflammatory cytokine transcriptional repressor, Oct-1, DNA-binding activities after chronic Ang II infusion and the effect of HS treatment on these pathways in heart.
  
  
  METHODS
  HS treatment was administered 24 hr before initiation of Ang II infusion to male Sprague-Dawley rats. Systolic blood pressure was measured by tail-cuff plethysmography, expression of heat shock proteins was monitored by Western analysis and DNA-binding activities of SP-1, AP-1 and Oct-1 were determined by electrophoretic mobility shift assay.
  
  
  RESULTS
  Ang II infusion induced a progressive increase in systolic blood pressure that was suppressed by the heat shock treatment. Following heat shock treatment, Hsp70 and Hsp27 were expressed at elevated levels. The Ang II-induced activation of SP-1 and AP-1 were significantly suppressed by HS treatment. In addition, HS increased Oct-1 activity that was suppressed by Ang II infusion.
  
  
  CONCLUSIONS
  These data suggest that heat shock suppresses inflammation by differentially regulating pro-inflammatory and anti-inflammatory cell signaling pathways.
authors.affiliation: Department of Anatomy & Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 1X5. wcurrie@dal.ca
authors.forename: Y
authors.initials: Y
authors.lastname: Chen
authors.forename: R W
authors.initials: RW
authors.lastname: Currie
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001794:Blood Pressure; D015153:Blotting, Western; D002467:Cell Nucleus / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism*; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006358:Hot Temperature; D006973:Hypertension; D007249:Inflammation; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism; D050811:Octamer Transcription Factor-1; D009841:Oligonucleotides / Q000737:chemistry; D011485:Protein Binding; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D016329:Sp1 Transcription Factor / Q000378:metabolism*; D013997:Time Factors; D018808:Transcription Factor AP-1 / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D004268:DNA-Binding Proteins; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C486114:Hspb1 protein, rat; D009363:Neoplasm Proteins; D050811:Octamer Transcription Factor-1; D009841:Oligonucleotides; C494168:Pou2f1 protein, rat; D016329:Sp1 Transcription Factor; D018808:Transcription Factor AP-1; D014157:Transcription Factors; D000804:Angiotensin II; D004247:DNA