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

Prostaglandins Leukot Essent Fatty Acids. 2009 Jul;81(1):31-3. doi: 10.1016/j.plefa.2009.05.019. Epub 2009 Jun 12.

Abstract

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 24h, 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 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.

MeSH terms

  • Animals
  • Benzyl Compounds / pharmacology
  • Creatine Kinase / blood
  • Epoprostenol / biosynthesis
  • Imidazoles / pharmacology
  • Intramolecular Oxidoreductases / deficiency*
  • Mice
  • Mice, Knockout
  • Myocardial Infarction / blood*
  • Myocardial Infarction / physiopathology
  • Myocardial Ischemia / physiopathology
  • Prostaglandin-E Synthases
  • Troponin I / blood

Substances

  • (2-(4-(4-isopropoxybenzyl)-phenylamino) imidazoline)
  • Benzyl Compounds
  • Imidazoles
  • Troponin I
  • Epoprostenol
  • Creatine Kinase
  • Intramolecular Oxidoreductases
  • Prostaglandin-E Synthases
  • Ptges protein, mouse