Modification of oxidative stress on gene expression profiling in the rat infarcted heart

Wenyuan Zhao, Tieqiang Zhao, Yuanjian Chen, Yanhua Qu, Ivan Gerling, Yao Sun

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Cardiac oxidative stress is developed following myocardial infarction (MI) particularly in the first week of MI. The influence of reactive oxygen species (ROS) on gene expression profiling and molecular pathways in the infarcted myocardium remains uncertain and is explored in the present study. Rats with MI were treated with or without antioxidants for 1 week. Normal rats served as controls. Cardiac oxidative stress and gene profiling were investigated. Compared to normal hearts, malondialdehyde, a marker of oxidative stress, was significantly increased in the infarcted myocardium, which was significantly suppressed by antioxidants. Microarray assay showed that over a thousand genes were differentially expressed in the infarcted myocardium. Antioxidants significantly altered the expression of 159 genes compared to untreated MI rats. Ingenuity pathway analysis indicated that multiple pathway networks were affected by antioxidants, including those related to cell movement, growth/development, death, and inflammatory/fibrotic responses. IPA further identified that these changes were primarily related to NFκB, p38 MAPK, and ERκ1/2 pathways. Hub genes were identified in the associated gene networks. This study reveals the gene networks associated with cardiac oxidative stress postMI. These observations indicate that ROS regulate various molecular and cellular actions related to cardiac repair/remodeling through multiple gene networks.

Original languageEnglish (US)
Pages (from-to)243-253
Number of pages11
JournalMolecular and Cellular Biochemistry
Volume379
Issue number1-2
DOIs
StatePublished - Jul 1 2013

Fingerprint

Oxidative stress
Gene Expression Profiling
Gene expression
Rats
Gene Regulatory Networks
Oxidative Stress
Antioxidants
Genes
Myocardial Infarction
Myocardium
Reactive Oxygen Species
p38 Mitogen-Activated Protein Kinases
Malondialdehyde
Growth and Development
Cell Movement
Gene Expression
Microarrays
Assays
Repair
Cells

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Modification of oxidative stress on gene expression profiling in the rat infarcted heart. / Zhao, Wenyuan; Zhao, Tieqiang; Chen, Yuanjian; Qu, Yanhua; Gerling, Ivan; Sun, Yao.

In: Molecular and Cellular Biochemistry, Vol. 379, No. 1-2, 01.07.2013, p. 243-253.

Research output: Contribution to journalArticle

Zhao, Wenyuan ; Zhao, Tieqiang ; Chen, Yuanjian ; Qu, Yanhua ; Gerling, Ivan ; Sun, Yao. / Modification of oxidative stress on gene expression profiling in the rat infarcted heart. In: Molecular and Cellular Biochemistry. 2013 ; Vol. 379, No. 1-2. pp. 243-253.
@article{779952c2ef91446d894ff0651c249512,
title = "Modification of oxidative stress on gene expression profiling in the rat infarcted heart",
abstract = "Cardiac oxidative stress is developed following myocardial infarction (MI) particularly in the first week of MI. The influence of reactive oxygen species (ROS) on gene expression profiling and molecular pathways in the infarcted myocardium remains uncertain and is explored in the present study. Rats with MI were treated with or without antioxidants for 1 week. Normal rats served as controls. Cardiac oxidative stress and gene profiling were investigated. Compared to normal hearts, malondialdehyde, a marker of oxidative stress, was significantly increased in the infarcted myocardium, which was significantly suppressed by antioxidants. Microarray assay showed that over a thousand genes were differentially expressed in the infarcted myocardium. Antioxidants significantly altered the expression of 159 genes compared to untreated MI rats. Ingenuity pathway analysis indicated that multiple pathway networks were affected by antioxidants, including those related to cell movement, growth/development, death, and inflammatory/fibrotic responses. IPA further identified that these changes were primarily related to NFκB, p38 MAPK, and ERκ1/2 pathways. Hub genes were identified in the associated gene networks. This study reveals the gene networks associated with cardiac oxidative stress postMI. These observations indicate that ROS regulate various molecular and cellular actions related to cardiac repair/remodeling through multiple gene networks.",
author = "Wenyuan Zhao and Tieqiang Zhao and Yuanjian Chen and Yanhua Qu and Ivan Gerling and Yao Sun",
year = "2013",
month = "7",
day = "1",
doi = "10.1007/s11010-013-1646-2",
language = "English (US)",
volume = "379",
pages = "243--253",
journal = "Molecular and Cellular Biochemistry",
issn = "0300-8177",
publisher = "Springer Netherlands",
number = "1-2",

}

TY - JOUR

T1 - Modification of oxidative stress on gene expression profiling in the rat infarcted heart

AU - Zhao, Wenyuan

AU - Zhao, Tieqiang

AU - Chen, Yuanjian

AU - Qu, Yanhua

AU - Gerling, Ivan

AU - Sun, Yao

PY - 2013/7/1

Y1 - 2013/7/1

N2 - Cardiac oxidative stress is developed following myocardial infarction (MI) particularly in the first week of MI. The influence of reactive oxygen species (ROS) on gene expression profiling and molecular pathways in the infarcted myocardium remains uncertain and is explored in the present study. Rats with MI were treated with or without antioxidants for 1 week. Normal rats served as controls. Cardiac oxidative stress and gene profiling were investigated. Compared to normal hearts, malondialdehyde, a marker of oxidative stress, was significantly increased in the infarcted myocardium, which was significantly suppressed by antioxidants. Microarray assay showed that over a thousand genes were differentially expressed in the infarcted myocardium. Antioxidants significantly altered the expression of 159 genes compared to untreated MI rats. Ingenuity pathway analysis indicated that multiple pathway networks were affected by antioxidants, including those related to cell movement, growth/development, death, and inflammatory/fibrotic responses. IPA further identified that these changes were primarily related to NFκB, p38 MAPK, and ERκ1/2 pathways. Hub genes were identified in the associated gene networks. This study reveals the gene networks associated with cardiac oxidative stress postMI. These observations indicate that ROS regulate various molecular and cellular actions related to cardiac repair/remodeling through multiple gene networks.

AB - Cardiac oxidative stress is developed following myocardial infarction (MI) particularly in the first week of MI. The influence of reactive oxygen species (ROS) on gene expression profiling and molecular pathways in the infarcted myocardium remains uncertain and is explored in the present study. Rats with MI were treated with or without antioxidants for 1 week. Normal rats served as controls. Cardiac oxidative stress and gene profiling were investigated. Compared to normal hearts, malondialdehyde, a marker of oxidative stress, was significantly increased in the infarcted myocardium, which was significantly suppressed by antioxidants. Microarray assay showed that over a thousand genes were differentially expressed in the infarcted myocardium. Antioxidants significantly altered the expression of 159 genes compared to untreated MI rats. Ingenuity pathway analysis indicated that multiple pathway networks were affected by antioxidants, including those related to cell movement, growth/development, death, and inflammatory/fibrotic responses. IPA further identified that these changes were primarily related to NFκB, p38 MAPK, and ERκ1/2 pathways. Hub genes were identified in the associated gene networks. This study reveals the gene networks associated with cardiac oxidative stress postMI. These observations indicate that ROS regulate various molecular and cellular actions related to cardiac repair/remodeling through multiple gene networks.

UR - http://www.scopus.com/inward/record.url?scp=84878436290&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84878436290&partnerID=8YFLogxK

U2 - 10.1007/s11010-013-1646-2

DO - 10.1007/s11010-013-1646-2

M3 - Article

VL - 379

SP - 243

EP - 253

JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

SN - 0300-8177

IS - 1-2

ER -