FASEB J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(The FASEB Journal. 2007;21:869.21)
© 2007 FASEB
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Buerke, M.
Right arrow Articles by Buerke, U.
PubMed
Right arrow Articles by Buerke, M.
Right arrow Articles by Buerke, U.

869.21

Aprotinin Exerts Inhibition of Gene Activation following Myocardial Ischemia and Reperfusion in Rats

Michael Buerke, Dennis Sankat, Axel Schlitt, Justin Carter, Karl Werdan and Ute Buerke

Dept of Medicine III, Martin-Luther-University, Ernst-Grube-Str. 40, Halle/Saale, 06097, Germany

ABSTRACT

Reperfusion of ischemic myocardium has been largely attributed to neutrophil infiltration with subsequent endothelial dysfunction, complement activation, cytokine release and cardiac apoptosis. Inhibition of serine proteases with aportinin has been shown to exert cardioprotective effects.

In this regard, we analyzed the effect of Aprotinin (Apro) in a rat model of myocardial ischemia and reperfusion (I.e., 20min + 24hours) on gene expression. Apro (20.000U/kg) administered 5 min prior to reperfusion significantly attenuated myocardial injury compared to vehicle treated rats (p<0.01). Further, cardiac myeloperoxidase activity, a marker for neutrophil accumulation was significantly reduced following Apro treatment (p<0.01). Further, analysis of differential gene expression was performed with labeled cDNA obtained from hearts following ischemia and reperfusion of vehicle or Apro treated animals (AtlasTM Rat cDNA Expression Array, Clontech). Ischemia and reperfusion resulted in expression of pro-inflammatory genes like P-selectin, MEK 2, JNK, STAT-3, N-myc, and c-jun as well as anti-inflammatory genes like MIF and MIP. Administration of Apro prior to reperfusion resulted in reduced expression of inflammatory genes as well as in enhanced expression of anti-inflammatory genes like heat shock protein 27, 60, and 70. When we performed protein analysis we were able to dermine reduced expression of p53, ICAM-1, p-selectin, IL-6, and TNF-alpha Thus, Apro appears to be an effective means to preserve ischemic myocardium from reperfusion injury due to reduced expression of pro-inflammatory genes even following 24 hours of reperfusion.





This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Buerke, M.
Right arrow Articles by Buerke, U.
PubMed
Right arrow Articles by Buerke, M.
Right arrow Articles by Buerke, U.