Cardiac release of urocortin precedes the occurrence of irreversible myocardial damage in the rat heart exposed to ischemia/reperfusion injury.

Abstract

This study evaluates whether cardiac ischemia induces release of urocortin, before and independently from myocyte cell death. Urocortin levels rose after 5-min ischemia and peaked after 10-min ischemia, when cell death was not detected. However, myocyte apoptosis and/or necrosis occurred following 20- and 30-min ischemia, which paralleled a fall in urocortin levels, suggesting that urocortin expression and release are mainly sustained by metabolically challenged, though still viable myocytes. Hence, since cardiac release of urocortin, unlike that of conventional biomarkers, occurs before and apart from cell death, urocortin levels may be clinically useful in the diagnosis of sublethal myocardial ischemia.

• Authors: Richard A Knight, Carol Chen-Scarabelli, Zhaokan Yuan, Roy B McCauley, J Di Rezze, Gabriele M Scarabelli, Paul A Townsend, David Latchman, Louis Saravolatz, Giuseppe Faggian, Alessandro Mazzucco, Hardial S Chowdrey, Anastasis Stephanou, Tiziano M Scarabelli
• Journal: FEBS letters (FEBS Lett) Vol. 582 Issue 6 Pg. 984-90 (Mar 19 2008) ISSN: 0014-5793 [Print] England
• PMID: 18295601 (Publication Type: Journal Article, Retracted Publication)

Chemical References

• Biomarkers
• Urocortins

Topics

• Animals
• Apoptosis
• Biomarkers (analysis, metabolism)
• Male
• Myocardial Reperfusion Injury (diagnosis, metabolism, pathology)
• Necrosis (diagnosis, metabolism, pathology)
• Rats
• Rats, Sprague-Dawley
• Urocortins (analysis, metabolism)