The heat shock paradox and cardiac myocytes: Role of heat shock factor

Samuel Kobba, Se Chan Kim, Le Chen, Eunjung Kim, Alice L. Tran, Pascal Knuefermann, Anne A Knowlton

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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°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 κB 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.

Original languageEnglish (US)
Pages (from-to)478-484
Number of pages7
JournalShock
Volume35
Issue number5
DOIs
StatePublished - May 2011

Fingerprint

Cardiac Myocytes
Shock
Hot Temperature
Wounds and Injuries
HSP72 Heat-Shock Proteins
Apoptosis
Chaperonin 60
Heat-Shock Response
Heme Oxygenase-1
Cell Survival
Inflammation
DNA

Keywords

  • apoptosis
  • HSF-1
  • HSP60
  • iNOS
  • MODS
  • NF-κB

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Emergency Medicine

Cite this

Kobba, S., Kim, S. C., Chen, L., Kim, E., Tran, A. L., Knuefermann, P., & Knowlton, A. A. (2011). The heat shock paradox and cardiac myocytes: Role of heat shock factor. Shock, 35(5), 478-484. https://doi.org/10.1097/SHK.0b013e3182094a0b

The heat shock paradox and cardiac myocytes : Role of heat shock factor. / Kobba, Samuel; Kim, Se Chan; Chen, Le; Kim, Eunjung; Tran, Alice L.; Knuefermann, Pascal; Knowlton, Anne A.

In: Shock, Vol. 35, No. 5, 05.2011, p. 478-484.

Research output: Contribution to journalArticle

Kobba, S, Kim, SC, Chen, L, Kim, E, Tran, AL, Knuefermann, P & Knowlton, AA 2011, 'The heat shock paradox and cardiac myocytes: Role of heat shock factor', Shock, vol. 35, no. 5, pp. 478-484. https://doi.org/10.1097/SHK.0b013e3182094a0b
Kobba S, Kim SC, Chen L, Kim E, Tran AL, Knuefermann P et al. The heat shock paradox and cardiac myocytes: Role of heat shock factor. Shock. 2011 May;35(5):478-484. https://doi.org/10.1097/SHK.0b013e3182094a0b
Kobba, Samuel ; Kim, Se Chan ; Chen, Le ; Kim, Eunjung ; Tran, Alice L. ; Knuefermann, Pascal ; Knowlton, Anne A. / The heat shock paradox and cardiac myocytes : Role of heat shock factor. In: Shock. 2011 ; Vol. 35, No. 5. pp. 478-484.
@article{0d9c26466cb64d7a9e1c709a4361e64f,
title = "The heat shock paradox and cardiac myocytes: Role of heat shock factor",
abstract = "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°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 κB 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.",
keywords = "apoptosis, HSF-1, HSP60, iNOS, MODS, NF-κB",
author = "Samuel Kobba and Kim, {Se Chan} and Le Chen and Eunjung Kim and Tran, {Alice L.} and Pascal Knuefermann and Knowlton, {Anne A}",
year = "2011",
month = "5",
doi = "10.1097/SHK.0b013e3182094a0b",
language = "English (US)",
volume = "35",
pages = "478--484",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - The heat shock paradox and cardiac myocytes

T2 - Role of heat shock factor

AU - Kobba, Samuel

AU - Kim, Se Chan

AU - Chen, Le

AU - Kim, Eunjung

AU - Tran, Alice L.

AU - Knuefermann, Pascal

AU - Knowlton, Anne A

PY - 2011/5

Y1 - 2011/5

N2 - 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°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 κB 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.

AB - 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°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 κB 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.

KW - apoptosis

KW - HSF-1

KW - HSP60

KW - iNOS

KW - MODS

KW - NF-κB

UR - http://www.scopus.com/inward/record.url?scp=79955548093&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79955548093&partnerID=8YFLogxK

U2 - 10.1097/SHK.0b013e3182094a0b

DO - 10.1097/SHK.0b013e3182094a0b

M3 - Article

C2 - 21192280

AN - SCOPUS:79955548093

VL - 35

SP - 478

EP - 484

JO - Shock

JF - Shock

SN - 1073-2322

IS - 5

ER -