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The heat shock paradox and cardiac myocytes: role of heat shock factor.

Authors: Kobba, S  Kim, SC  Chen, L  Kim, E  Tran, AL  Knuefermann, P  Knowlton, AA 
Citation: Kobba S, etal., Shock. 2011 May;35(5):478-84. doi: 10.1097/SHK.0b013e3182094a0b.
Pubmed: (View Article at PubMed) PMID:21192280
DOI: Full-text: DOI:10.1097/SHK.0b013e3182094a0b

The induction of the heat shock (HS) response is accepted to be a protective response, reducing injury and improving cell survival. However, when inflammation precedes HS, there is an unexpected increase in injury, known as the HS paradox, which is hypothesized to be a mechanism underlying multiorgan dysfunction. We hypothesized that the HS paradox would occur in adult cardiac myocytes and that HS factor (HSF) 1 would contribute to injury. Heat shock at 42 degrees C and TNF (10 ng/mL) were used as the HS and the inflammatory insult, respectively. The combination of TNF followed by HS (TNF/HS) caused the greatest amount of apoptosis in adult rat cardiac myocytes. TNF/HS resulted in an increase in HS protein (HSP) 60, compared with untreated cells, those receiving HS/TNF, or TNF alone. There was no increase in heme oxygenase 1 in any of the groups. Heat shock protein 72 increased in all the groups, with the greatest levels with TNF/HS. Nuclear factor kappaB activation was greatest with TNF/HS. Pretreatment with a DNA-binding decoy for HSF-1 prevented the increase in HSPs and decreased apoptosis in all groups. However, the increase in iNOS, seen in all treatment groups, was unaffected by the HSF-1-binding decoy. We conclude that the HS paradox occurs in adult cardiac myocytes, that HSP60 is increased as part of the HS paradox, and that HSF-1 activation contributes to injury.


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CRRD Object Information
CRRD ID: 10403035
Created: 2015-11-04
Species: All species
Last Modified: 2015-11-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.