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Early Biventricular Molecular Responses to an Acute Myocardial Infarction
Background: 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....
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Ivyspring International Publisher
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245415/ https://www.ncbi.nlm.nih.gov/pubmed/22211093 |
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author | Erdal, Cenk Karakülah, Gökhan Fermancı, Emel Kunter, İmge Silistreli, Erdem Canda, Tülay Erdal, Esra Hepaguslar, Hasan |
author_facet | Erdal, Cenk Karakülah, Gökhan Fermancı, Emel Kunter, İmge Silistreli, Erdem Canda, Tülay Erdal, Esra Hepaguslar, Hasan |
author_sort | Erdal, Cenk |
collection | PubMed |
description | Background: 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. Objectives: The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI. Material and Methods: 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. Results: 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. Conclusion: 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. |
format | Online Article Text |
id | pubmed-3245415 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-32454152012-01-01 Early Biventricular Molecular Responses to an Acute Myocardial Infarction Erdal, Cenk Karakülah, Gökhan Fermancı, Emel Kunter, İmge Silistreli, Erdem Canda, Tülay Erdal, Esra Hepaguslar, Hasan Int J Med Sci Research Paper Background: 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. Objectives: The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI. Material and Methods: 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. Results: 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. Conclusion: 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. Ivyspring International Publisher 2011-11-30 /pmc/articles/PMC3245415/ /pubmed/22211093 Text en © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. |
spellingShingle | Research Paper Erdal, Cenk Karakülah, Gökhan Fermancı, Emel Kunter, İmge Silistreli, Erdem Canda, Tülay Erdal, Esra Hepaguslar, Hasan Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title | Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title_full | Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title_fullStr | Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title_full_unstemmed | Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title_short | Early Biventricular Molecular Responses to an Acute Myocardial Infarction |
title_sort | early biventricular molecular responses to an acute myocardial infarction |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245415/ https://www.ncbi.nlm.nih.gov/pubmed/22211093 |
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