AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 280: H426-H433, 2001;
0363-6135/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chang, J.
Right arrow Articles by Wasser, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chang, J.
Right arrow Articles by Wasser, J. S.
Vol. 280, Issue 1, H426-H433, January 2001

Activation of the heat shock response: relationship to energy metabolites. A 31P NMR study in rat hearts

J. Chang1, A. A. Knowlton2, F. Xu1, and J. S. Wasser1

1 Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station 77843; and 2 Baylor College of Medicine and Veterans Affairs Medical Center, Houston, TX 77030

Heat shock factor (HSF), the transcription factor for the heat shock proteins, is activated by cardiac ischemia, but the mechanism of activation is unknown. Ischemia is accompanied by changes in the energy state and acid-base conditions. We hypothesized that decreased ATP and/or intracellular pH (pHi) might activate HSF. To test this hypothesis, we perfused rat hearts within an NMR spectrometer. NMR data showed that after 6.5, 13, and 20 min of ischemia, ATP dropped to 62.7, 23.1, and 6.9% of the control level, and pHi was 6.16, 5.94, and 5.79, respectively. Reperfusion after ischemia partially restored ATP levels, and this was associated with greater activation of HSF1. HSF1 was also activated after 6.5 min of ischemia. Activation of HSF1 was less after 13 min of ischemia and barely detectable after 20 min of ischemia. In conclusion, 1) a moderate decrease in intracellular ATP correlates with activation of HSF1 in the heart; and 2) a severe depletion in ATP correlates with an attenuation in HSF1 activation, and the restoration of ATP leads to greater activation of HSF1, suggesting that a critical ATP level is required for activation of HSF1.

heat shock factor 1; intracellular pH; ATP; free energy of ATP hydrolysis; ischemia; reperfusion; rat heart; cardiac energetics


This article has been cited by other articles:


Home page
 IOVSHome page
N. A. Whitlock, N. Agarwal, J.-X. Ma, and C. E. Crosson
Hsp27 Upregulation by HIF-1 Signaling Offers Protection against Retinal Ischemia in Rats
Invest. Ophthalmol. Vis. Sci., March 1, 2005; 46(3): 1092 - 1098.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
X.-H. Ning, S.-H. Chen, C.-S. Xu, O. M. Hyyti, K. Qian, J. J. Krueger, and M. A. Portman
Hypothermia preserves myocardial function and mitochondrial protein gene expression during hypoxia
Am J Physiol Heart Circ Physiol, June 5, 2003; 285(1): H212 - H219.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
J. Chang, J. S. Wasser, R. N.M. Cornelussen, and A.A. Knowlton
Activation of Heat-Shock Factor by Stretch-Activated Channels in Rat Hearts
Circulation, July 10, 2001; 104(2): 209 - 214.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online