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B pathway and heart inflammation: A role for IKK depletion by heat shock?
1 Department of Anatomy & Neurobiology, Dalhousie University, Halifax, NS B3H 1X5, Canada
2 Laboratoire stress oxidant, chaperons et apoptose, Centre de Genetique Moleculaire et Cellulaire, CNRS UMR-5534, Universite Claude Bernard Lyon-1, Villeurbanne, 69622, France
3 Department of Anatomy & Neurobiology, Dalhousie University, Halifax, NS B3H 1X5, Canada; Laboratoire stress oxidant, chaperons et apoptose, Centre de Genetique Moleculaire et Cellulaire, CNRS UMR-5534, Universite Claude Bernard Lyon-1, Villeurbanne, 69622, France
* To whom correspondence should be addressed. E-mail: wcurrie{at}dal.ca.
Heat shock proteins function in tissue protection through their chaperone activity and by interacting with cell signaling pathways to suppress apoptosis. Here we investigated the effect of heat shock (HS) treatment on the NF-
B signaling pathway in the Angiotensin II (Ang II) model of inflammation. Male Sprague-Dawley rats were divided into sham, HS, Ang II and HS+Ang II treated groups. HS treatment was administered 24 hr before initiation of Ang II infusion. HS treatment (42°C for 15 min) decreased 7 day Ang II induced hypertension from 191±4 mm Hg to 147±3 mm Hg (p<0.01). Histological staining of hearts showed that HS treatment reduced Ang II induced leukocyte infiltration, perivascular and interstitial inflammation and fibrosis. Heart
NF-B nuclear translocation and activity, examined by Western analysis and electrophoretic
mobility shift assay, was suppressed by HS treatment. HS treatment depleted IB kinase-
(IKK-) and phosphorylated IKK- and suppressed the depletion of IB- and the accumulation of phosphorylated IB-. HS treatment blocked Ang II induced expression of IL-6 and ICAM-1 in the heart. Ang II and HS treatment induced high level expression of Hsp27 and Hsp70 and their phosphorylation. Phosphorylated isoforms of Hsp27 and Hsp70 may play an important role in protecting the heart against Angiotensin II-induced inflammation.
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