Linked Life Data

14734055

Source:http://linkedlifedata.com/resource/pubmed/id/14734055

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-1-21
pubmed:abstractText
In a variety of vascular disorders, endothelial cells (ECs) are exposed to high levels of reactive oxygen species (ROS) generated intercellularly. Recently, several anti-oxidants, including catalase, have been suggested to be cytoprotective against the development of atherosclerosis. The object of this study was to investigate whether adenovirus-mediated gene transfer of catalase in ECs can attenuate ROS production and cell apoptosis under oxidized low density lipoprotein (oxLDL) stimulation. Adenovirus-mediated gene transfer of human catalase gene (Ad-Cat) resulted in a high level of catalase overexpression in human arterial EC (HAEC), which manifested a time-dependent increase in cell viability under the exposure of oxLDL and decreased oxLDL-induced apoptosis. Phosphorylation studies of ERK1/2, JNK, and p38, three subgroups of mitogen activator protein kinase demonstrated that catalase overexpression suppressed JNK phosphorylation and increased ERK1/2 phosphorylation. NF-kappaB and AP-1 were induced after the exposure of HAECs to oxLDL. While catalase overexpression was found to inactivate AP-1, it had no effect on NF-kappaB activity. These results provide the evidence that overexpression of catalase in ECs attenuates ROS production and cell apoptosis under oxLDL stimulation. The protective effect is mediated through the downregulation of JNK and the upregulation of ERK1/2 phosphorylation as well as AP-1 inactivation. This observation supports the feasibility of catalase gene transfer to human endothelium to protect against oxidant injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-39
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14734055-Adenoviridae, pubmed-meshheading:14734055-Aorta, pubmed-meshheading:14734055-Apoptosis, pubmed-meshheading:14734055-Catalase, pubmed-meshheading:14734055-Cell Survival, pubmed-meshheading:14734055-Electrophoretic Mobility Shift Assay, pubmed-meshheading:14734055-Endothelial Cells, pubmed-meshheading:14734055-Gene Expression Profiling, pubmed-meshheading:14734055-Genetic Vectors, pubmed-meshheading:14734055-Humans, pubmed-meshheading:14734055-Hydrogen Peroxide, pubmed-meshheading:14734055-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:14734055-Lipoproteins, LDL, pubmed-meshheading:14734055-MAP Kinase Signaling System, pubmed-meshheading:14734055-Mitogen-Activated Protein Kinases, pubmed-meshheading:14734055-NF-kappa B, pubmed-meshheading:14734055-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:14734055-Phosphorylation, pubmed-meshheading:14734055-Transcription Factor AP-1
pubmed:year
2004
pubmed:articleTitle
Adenovirus-mediated overexpression of catalase attenuates oxLDL-induced apoptosis in human aortic endothelial cells via AP-1 and C-Jun N-terminal kinase/extracellular signal-regulated kinase mitogen-activated protein kinase pathways.
pubmed:affiliation
Institute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't