scholarly journals Cytosolic heat shock protein 90 regulates heat shock transcription factor inArabidopsis thaliana

2008 ◽  
Vol 3 (9) ◽  
pp. 660-662 ◽  
Author(s):  
Kenji Yamada ◽  
Mikio Nishimura
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 90 ◽  
Heat Shock Transcription Factor

Increased temperature, not cardiac load, activates heat shock transcription factor 1 and heat shock protein 72 expression in the heart

2007 ◽  
Vol 292 (1) ◽  
pp. R432-R439 ◽  
Author(s):  
Jessica L. Staib ◽  
John C. Quindry ◽  
Joel P. French ◽  
David S. Criswell ◽  
Scott K. Powers
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Nuclear Translocation ◽  
Mechanical Load ◽  
Left Ventricular ◽  
Heat Shock Transcription Factor ◽  
Heat Shock Protein 72 ◽  
Increased Temperature ◽  
Transcription Factor 1

The expression of myocardial heat shock protein 72 (HSP72) postexercise is initiated by the activation of heat shock transcription factor 1 (HSF1). However, it remains unknown which physiological stimuli govern myocardial HSF1 activation during exercise. These experiments tested the hypothesis that thermal stress and mechanical load, concomitant with simulated exercise, provide independent stimuli for HSF1 activation and ensuing cardiac HSP72 gene expression. To elucidate the independent roles of increased temperature and cardiac workload in the exercise-mediated upregulation of left-ventricular HSP72, hearts from adult male Sprague-Dawley rats were randomly assigned to one of five simulated exercise conditions. Upon reaching a surgical plane of anesthesia, each experimental heart was isolated and perfused using an in vitro working heart model, while independently varying temperatures (i.e., 37°C vs. 40°C) and cardiac workloads (i.e., low preload and afterload vs. high preload and afterload) to mimic exercise responses. Results indicate that hyperthermia, independent of cardiac workload, promoted an increase in nuclear translocation and phosphorylation of HSF1 compared with normothermic left ventricles. Similarly, hyperthermia, independent of workload, resulted in significant increases in cardiac levels of HSP72 mRNA. Collectively, these data suggest that HSF1 activation and HSP72 gene transcriptional competence during simulated exercise are linked to elevated heart temperature and are not a direct function of increased cardiac workload.

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