Journal
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Volume 81, Issue 1, Pages 31-33Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.plefa.2009.05.019
Keywords
Microsomal prostaglandin E synthase-1; Prostaglandin E-2; Myocardial ischemia; Prostacyclin I-2
Funding
- Boehringer Ingelheim Pharma GmbH & Co. KG, Germany
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The goal of the present study was to assess how genetic loss of microsomal prostaglandin E-2 synthase-1 (mPGES-1) affects acute cardiac ischemic damage after coronary occlusion in mice. Wild type (WT), heterozygous (mPGES-1(+/-)), and homozygous (mPGES-1(-/-)) knockout mice were subjected to left coronary artery occlusion. At 24 h, myocardial infarct (MI) volume was measured histologically. Post-MI survival, plasma levels of creatine phosphokinase (CPK) and cardiac troponin-1 together with MI size, were similar in WT, mPGES-1(+/-) and mPGES-1(-/-) mice. In contrast, post-Ml survival was reduced in mPGES-1(-/-) mice pretreated with I prostanoid receptor (IP) antagonist (12/16) compared with vehicle-treated controls (13/13 mPGES-1(-/-)) together with increased CPK and cardiac troponin-I release. The deletion of mPGES-1 in mice results in increased prostacyclin I-2 (PGI(2)) formation and marginal effects on the circulatory prostaglandin E-2 (PGE(2)) level. We conclude that loss of mPGES-1 results in increased PGI(2) formation, and in contrast to inhibition of PGI(2), without worsening acute cardiac ischemic injury. (C) 2009 Elsevier Ltd. All rights reserved.
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