Early Biventricular Molecular Responses to an Acute Myocardial Infarction

• Main Author: Cenk Erdal, Gökhan Karakülah, Emel Fermancı, İmge Kunter, Erdem Silistreli, Tülay Canda, Esra Erdal, Hasan Hepaguslar
• Format: Article
• Language: English
• Published: Ivyspring International Publisher 2012-01-01
• Series: International Journal of Medical Sciences
• Online Access: http://www.medsci.org/v09p0074.htm

<p><b>Background: </b>Acute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose.</p><p><b>Objectives: </b>The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI.</p><p><b>Material and Methods:</b> A rat model of left anterior descending coronary artery ligation was used to assess the effect of left ventricular AMI on both the right ventricle as a remote zone and the left ventricle as an ischemic/infarct zone. Microarray technology was applied to detect the gene expression. Gene Ontology and KEGG pathways analysis were done to identify effected pathways and related genes.</p><p><b>Results: </b>We found that immune response, cell chemotaxis, inflammation, cytoskeleton organization are significantly deregulated in ischemic zone as early response within 30 min. Unexpectedly, there were several affected signaling pathways such as cell chemotaxis, regulation of endothelial cell proliferation, and regulation of caveolea regulation of anti-apoptosis, regulation of cytoskeleton organization and cell adhesion on the remote zone in the right ventricle.</p><p><b>Conclusion: </b>This data demonstrates that there is an immediate molecular response in both ventricles after an AMI. Although the ischemia did not histologically involve the right ventricle; there is a clear molecular response to the infarct in the left ventricle. This provides us new insights to understand molecular mechanisms behind AMI and to find more effective drug targets.</p>