Comparison of microsomal prostaglandin E synthase-1 deletion and COX-2 inhibition in acute cardiac ischemia in mice

Prostaglandins Other Lipid Mediat. 2009 Nov;90(1-2):21-5. doi: 10.1016/j.prostaglandins.2009.06.006. Epub 2009 Jun 25.

Abstract

The aim of the present study was to compare the effects of genetic mPGES-1 loss and COX-2 inhibition on myocardial damage after coronary occlusion. mPGES-1(-/-) mice and their wild-type littermates were injected with vehicle or COX-2 inhibitor (celecoxib), and 30min later the left coronary artery was surgically occluded. At 24h, myocardial infarct (MI) volume was measured histologically. Post-MI survival was reduced in WT mice receiving celecoxib (12/20) compared with vehicle-treated controls (12/12) or the loss of mPGES-1 (13/13) together with increased phosphokinase (CPK) and cardiac troponin-I release. Endogenous mPGES-1 expression was unchanged by ischemia in WT mice and absent in mPGES-1(-/-) hearts. COX-2 expression was markedly increased at 24h after MI in WT hearts; this upregulation was largely attenuated in mPGES-1(-/-) mice. We conclude that loss of mPGES-1 prevents the upregulation of COX-2 after myocardial infarct, and in contrast to inhibition of COX-2, does not increase ischemic myocardial damage.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Coronary Occlusion / complications
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Gene Deletion*
  • Gene Expression Regulation, Enzymologic
  • Intramolecular Oxidoreductases / deficiency*
  • Intramolecular Oxidoreductases / genetics*
  • Mice
  • Microsomes / enzymology*
  • Myocardial Infarction / complications
  • Myocardial Infarction / pathology
  • Myocardial Ischemia / complications
  • Myocardial Ischemia / enzymology*
  • Myocardial Ischemia / genetics*
  • Myocardial Ischemia / pathology
  • Prostaglandin-E Synthases
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism

Substances

  • Cyclooxygenase 2 Inhibitors
  • RNA, Messenger
  • Cyclooxygenase 2
  • Intramolecular Oxidoreductases
  • Prostaglandin-E Synthases
  • Ptges protein, mouse