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 282: H1461-H1466, 2002; doi:10.1152/ajpheart.00447.2001
0363-6135/02 $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 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 Web of Science (16)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Temsah, R. M.
Right arrow Articles by Dhalla, N. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Temsah, R. M.
Right arrow Articles by Dhalla, N. S.
Vol. 282, Issue 4, H1461-H1466, April 2002

Preconditioning prevents alterations in cardiac SR gene expression due to ischemia-reperfusion

Rana M. Temsah, Kenichi Kawabata, Donald Chapman, and Naranjan S. Dhalla

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6

We have previously shown that ischemic preconditioning (IP) improves cardiac performance and sarcoplasmic reticulum (SR) function in hearts subjected to ischemia-reperfusion (I/R). In this study, we examined the effect of IP on I/R-induced changes in gene expression for SR proteins such as the Ca2+ release channel, Ca2+ pump ATPase, phospholamban, and calsequestrin in the isolated rat heart. Normal isolated rat hearts exposed to three brief cycles of IP (5-min ischemia and 5-min reperfusion) exhibited a significant decrease in the transcript levels of SR genes. Nonpreconditioned I/R hearts when subjected to 30-min ischemia and 30-min reperfusion showed a marked decrease in mRNA levels for the SR proteins compared with normal hearts; this decrease was attenuated by preconditioning. Although hearts subjected to Ca2+ paradox (CP) have been shown to exhibit intracellular Ca2+ overload and SR dysfunction like those in I/R hearts, virtually nothing is known regarding the effect of CP on cardiac SR gene expression. Accordingly, CP (5-min Ca2+-free perfusion and 30-min reperfusion with normal medium) was observed to produce dramatic changes in SR gene expression, and the heart failed to contract; these alterations were attenuated by IP. Our results show that 1) both I/R and CP depress SR gene expression in the normal heart, 2) IP attenuates I/R- and CP-induced depression in cardiac function and SR gene expression, and 3) intracellular Ca2+ overload may play a role in depressing SR gene expression in both I/R and CP hearts.

ischemic preconditioning; ischemia-reperfusion; cardiac mRNA levels; Ca2+ paradoxic heart


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
S. Morales, A. Diez, A. Puyet, P. J. Camello, C. Camello-Almaraz, J. M. Bautista, and M. J. Pozo
Calcium controls smooth muscle TRPC gene transcription via the CaMK/calcineurin-dependent pathways
Am J Physiol Cell Physiol, January 1, 2007; 292(1): C553 - C563.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
Y.-J. Xu, H. K. Saini, M. Zhang, V. Elimban, and N. S. Dhalla
MAPK activation and apoptotic alterations in hearts subjected to calcium paradox are attenuated by taurine
Cardiovasc Res, October 1, 2006; 72(1): 163 - 174.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
L. Chen, X.-Y. Lu, J. Li, J.-D. Fu, Z.-N. Zhou, and H.-T. Yang
Intermittent hypoxia protects cardiomyocytes against ischemia-reperfusion injury-induced alterations in Ca2+ homeostasis and contraction via the sarcoplasmic reticulum and Na+/Ca2+ exchange mechanisms
Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1221 - C1229.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
S. Takeda, S. Mochizuki, H. K. Saini, V. Elimban, and N. S. Dhalla
Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts
J Appl Physiol, September 1, 2005; 99(3): 999 - 1005.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
H. K. Saini, V. Elimban, and N. S. Dhalla
Attenuation of extracellular ATP response in cardiomyocytes isolated from hearts subjected to ischemia-reperfusion
Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H614 - H623.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Zhang, Y.-J. Xu, H. K. Saini, B. Turan, P. P. Liu, and N. S. Dhalla
Pentoxifylline attenuates cardiac dysfunction and reduces TNF-{alpha} level in ischemic-reperfused heart
Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H832 - H839.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Xie, Y. Zhu, W.-Z. Zhu, L. Chen, Z.-N. Zhou, W.-J. Yuan, and H.-T. Yang
Role of dual-site phospholamban phosphorylation in intermittent hypoxia-induced cardioprotection against ischemia-reperfusion injury
Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2594 - H2602.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
H. K. Saini and N. S. Dhalla
Defective calcium handling in cardiomyocytes isolated from hearts subjected to ischemia-reperfusion
Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2260 - H2270.
[Abstract] [Full Text] [PDF]


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