p38 MAPK activity is not increased early during sustained coronary artery occlusion in preconditioned versus control rabbit heart

Anne Gysembergh, Boris Z. Simkhovich, Robert A. Kloner, Karin Przyklenk

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Our aim was to test the hypothesis that cardioprotection achieved with ischemic preconditioning (PC) involves increased activity of p38 mitogen-activated protein kinase (MAPK) early during sustained coronary artery occlusion. Using the isolated buffer-perfused rabbit heart model of regional ischemia, we quantified p38 MAPK activity (pmol/min/mg protein: by biochemical assay) at 5 and 10 min into coronary occlusion in hearts that first received PC ischemia or no intervention (controls). and in non-ischemic shams. Control hearts exhibited significant increases in p38 MAPK activity, averaging 883 ± 142 and 1135 ± 179 at 5 and 10 min of occlusion. ν 144 ± 49 in shams (P<0.05 and P<0.01). p38 MAPK activity was not, however, augmented with PC: rather, at 5 min into occlusion, activity was attenuated, averaging 432 ± 72 (P=N.S. ν sham). This early, modest reduction in p38 MAPK activity may be physiologically relevant: in additional hearts subjected to 30 min of sustained coronary occlusion and 2 h of reperfusion, infarct size (by tetrazolium staining: expressed as a % of the risk region) was 54 ± 5% in hearts treated with SB 203580 (confirmed in our study to inhibit p38 MAPK activity at 5 min into occlusion) ν 70 ± 5% in vehicle controls (P<0.05). Thus, cardioprotection achieved with ischemic preconditioning in rabbit heart does not involve augmentation of p38 MAPK activity early during sustained coronary occlusion.

Original languageEnglish
Pages (from-to)681-690
Number of pages10
JournalJournal of Molecular and Cellular Cardiology
Volume33
Issue number4
DOIs
StatePublished - 2001

Keywords

  • Cardioprotection
  • Mitogen-activated protein kinase
  • Myocardial infarction
  • Myocardial ischemia
  • Signal transduction

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