The effects of microsomal prostaglandin E synthase-1 deletion in acute cardiac ischemia in mice

Dongmei Wu, Detlev Mennerich, Kirsten Arndt, Kenji Sugiyama, Naoko Ozaki, Karoline Schwarz, Jianqin Wei, Heng Wu, Nanette H. Bishopric, Henri Doods

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


The goal of the present study was to assess how genetic loss of microsomal prostaglandin E2 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-I, together with MI size, were similar in WT, mPGES-1+/- and mPGES-1-/- mice. In contrast, post-MI 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 I2 (PGI2) formation and marginal effects on the circulatory prostaglandin E2 (PGE2) level. We conclude that loss of mPGES-1 results in increased PGI2 formation, and in contrast to inhibition of PGI2, without worsening acute cardiac ischemic injury.

Original languageEnglish (US)
Pages (from-to)31-33
Number of pages3
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Issue number1
StatePublished - Jul 2009


  • Microsomal prostaglandin E synthase-1
  • Myocardial ischemia
  • Prostacyclin I
  • Prostaglandin E

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry


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