Heat shock treatment suppresses angiotensin II-induced SP-1 and AP-1 and stimulates Oct-1 DNA-binding activity in heart.

OBJECTIVE AND
DESIGN: 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.
CONCLUSION: These data suggest that heat shock suppresses inflammation by differentially regulating pro-inflammatory and anti-inflammatory cell signaling pathways.