Skip Navigation

Cardiovascular Research 2002 55(3):495-505; doi:10.1016/S0008-6363(02)00337-1
© 2002 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Hoshida, S.
Right arrow Articles by Hori, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoshida, S.
Right arrow Articles by Hori, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

The importance of manganese superoxide dismutase in delayed preconditioning

Involvement of reactive oxygen species and cytokines

Shiro Hoshidaa,b,*, Nobushige Yamashitaa, Kinya Otsua and Masatsugu Horia

aDepartment of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Osaka 591-8025, Japan
bDivision of Cardiology, Osaka Rosai Hospital, 1179-3, Nagasone-cho, Sakai, Japan

hoshidas{at}orh.go.jp

* Corresponding author. Tel.: +81-72-252-3561; fax: +81-72-250-5492

It is clinically important to elucidate the mechanism underlying the delayed preconditioning against ischemia–reperfusion injury observed 24–72 h after sublethal stress such as brief ischemia, hyperthermia and exercise. The time course of induction of myocardial manganese-superoxide dismutase (Mn-SOD) and appearance of the ischemic tolerance coincide well, and the percent increase in Mn-SOD activity and percent reduction of infarct size are correlated well under various stresses. Furthermore, treatments with antisense oligodeoxynucleotides to Mn-SOD completely abolished the delayed preconditioning and any increase in Mn-SOD content. These results indicate that Mn-SOD induction plays a pivotal role in the late phase preconditioning afforded with brief ischemia, hyperthermia and exercise. We also showed that cytokines, e.g., tumor necrosis factor-{alpha} and interleukin-1β, and reactive oxygen species are involved in the process of signal transduction for the Mn-SOD induction.

KEYWORDS Cytokines; Ischemia; Preconditioning


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
M. Hori and K. Nishida
Oxidative stress and left ventricular remodelling after myocardial infarction
Cardiovasc Res, February 15, 2009; 81(3): 457 - 464.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
D. A. Brown and R. L. Moore
Perspectives in innate and acquired cardioprotection: cardioprotection acquired through exercise
J Appl Physiol, November 1, 2007; 103(5): 1894 - 1899.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
H. Sato, R. Bolli, G. D. Rokosh, Q. Bi, S. Dai, G. Shirk, and X.-L. Tang
The cardioprotection of the late phase of ischemic preconditioning is enhanced by postconditioning via a COX-2-mediated mechanism in conscious rats
Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2557 - H2564.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
S. Koneru, S. V. Penumathsa, M. Thirunavukkarasu, S. M. Samuel, L. Zhan, Z. Han, G. Maulik, D. K. Das, and N. Maulik
Redox regulation of ischemic preconditioning is mediated by the differential activation of caveolins and their association with eNOS and GLUT-4
Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2060 - H2072.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
F. Kolar, J. Jezkova, P. Balkova, J. Breh, J. Neckar, F. Novak, O. Novakova, H. Tomasova, M. Srbova, B. Ost'adal, et al.
Role of oxidative stress in PKC-{delta} upregulation and cardioprotection induced by chronic intermittent hypoxia
Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H224 - H230.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
H. J. Zhang, S. R. Doctrow, L. W. Oberley, and K. C. Kregel
Chronic antioxidant enzyme mimetic treatment differentially modulates hyperthermia-induced liver HSP70 expression with aging
J Appl Physiol, April 1, 2006; 100(4): 1385 - 1391.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
Z.-Q. Jin, H.-Z. Zhou, G. Cecchini, M. O. Gray, and J. S. Karliner
MnSOD in mouse heart: acute responses to ischemic preconditioning and ischemia-reperfusion injury
Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2986 - H2994.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
D. B. Buxton
Cytokines and Late Preconditioning
Cardiovasc Res, October 1, 2004; 64(1): 6 - 8.
[Full Text] [PDF]


Home page
Cardiovasc ResHome page
Y. Nishino, T. Miura, T. Miki, J. Sakamoto, Y. Nakamura, Y. Ikeda, H. Kobayashi, and K. Shimamoto
Ischemic preconditioning activates AMPK in a PKC-dependent manner and induces GLUT4 up-regulation in the late phase of cardioprotection
Cardiovasc Res, February 15, 2004; 61(3): 610 - 619.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
D. M Yellon and J. M Downey
Spotlight on preconditioning
Cardiovasc Res, August 15, 2002; 55(3): 425 - 428.
[Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.