Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery

DSpace/Manakin Repository

Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery

Citable link to this page

. . . . . .

Title: Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery
Author: Adachi, Masaaki; Liu, Yaohua; Fujii, Kyoko; Nakai, Akira; Imai, Kohzoh; Shinomura, Yasuhisa; Calderwood, Stuart K.

Note: Order does not necessarily reflect citation order of authors.

Citation: Adachi, Masaaki, Yaohua Liu, Kyoko Fujii, Stuart K. Calderwood, Akira Nakai, Kohzoh Imai, and Yasuhisa Shinomura. 2009. Oxidative stress impairs the heat stress response and delays unfolded protein recovery. PLoS ONE 4(11): e7719.
Full Text & Related Files:
Abstract: Background: Environmental changes, air pollution and ozone depletion are increasing oxidative stress, and global warming threatens health by heat stress. We now face a high risk of simultaneous exposure to heat and oxidative stress. However, there have been few studies investigating their combined adverse effects on cell viability. Principal Findings: Pretreatment of hydrogen peroxide \((H_2O_2\)) specifically and highly sensitized cells to heat stress, and enhanced loss of mitochondrial membrane potential. \(H_2O_2\) exposure impaired the HSP40/HSP70 induction as heat shock response (HSR) and the unfolded protein recovery, and enhanced \(eIF2\alpha\) phosphorylation and/or XBP1 splicing, land marks of ER stress. These \(H_2O_2\)-mediated effects mimicked enhanced heat sensitivity in HSF1 knockdown or knockout cells. Importantly, thermal preconditioning blocked \(H_2O_2\)–mediated inhibitory effects on refolding activity and rescued HSF1 +/+ MEFs, but neither blocked the effects nor rescued HSF1 -/- MEFs. These data strongly suggest that inhibition of HSR and refolding activity is crucial for \(H_2O_2\)–mediated enhanced heat sensitivity. Conclusions: \(H_2O_2\) blocks HSR and refolding activity under heat stress, thereby leading to insufficient quality control and enhancing ER stress. These uncontrolled stress responses may enhance cell death. Our data thus highlight oxidative stress as a crucial factor affecting heat tolerance.
Published Version: doi://10.1371/journal.pone.0007719
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777389/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4930626

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters