Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2005-6-10
pubmed:abstractText
Increased oxidative stress in vascular cells plays a key role in the development of endothelial dysfunction and atherosclerosis. Uncoupling protein 2 (UCP2) is an important regulator of intracellular reactive oxygen species (ROS) production. This study was undertaken to test the hypothesis that, UCP2 functions as an inhibitor of the atherosclerotic process in endothelial cells. Adenovirus-mediated UCP2 (Ad-UCP2) overexpression led to a significant increase in endothelial nitric oxide synthase (eNOS) and decrease in endothelin-1 mRNA expression in human aortic endothelial cells (HAECs). Moreover, UCP2 inhibited the increase in ROS production and NF-kappaB activation, and apoptosis of HAECs induced by lysophophatidylcholine (LPC) and linoleic acid. LPC and linoleic acid caused mitochondrial calcium accumulation and transient mitochondrial membrane hyperpolarization, which was followed by depolarization. UCP2 overexpression prevented these processes. In isolated rat aorta, Ad-UCP2 infection markedly improved impaired vascular relaxation induced by LPC. The data collectively suggest that UCP2, functions as a physiologic regulator of ROS generation in endothelial cells. Thus, measures to increase UCP2 expression in vascular endothelial cells may aid in preventing the development and progression of atherosclerosis in patients with metabolic syndrome.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Caspases, http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1, http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels, http://linkedlifedata.com/resource/pubmed/chemical/Linoleic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Lysophosphatidylcholines, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Transport Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins, http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B, http://linkedlifedata.com/resource/pubmed/chemical/NOS3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species, http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 2
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1200-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15905464-Adenoviridae, pubmed-meshheading:15905464-Apoptosis, pubmed-meshheading:15905464-Arteriosclerosis, pubmed-meshheading:15905464-Calcium, pubmed-meshheading:15905464-Caspases, pubmed-meshheading:15905464-Cells, Cultured, pubmed-meshheading:15905464-Electron Transport, pubmed-meshheading:15905464-Endothelial Cells, pubmed-meshheading:15905464-Endothelin-1, pubmed-meshheading:15905464-Gene Transfer, Horizontal, pubmed-meshheading:15905464-Humans, pubmed-meshheading:15905464-Ion Channels, pubmed-meshheading:15905464-Linoleic Acid, pubmed-meshheading:15905464-Lysophosphatidylcholines, pubmed-meshheading:15905464-Membrane Transport Proteins, pubmed-meshheading:15905464-Mitochondrial Proteins, pubmed-meshheading:15905464-NF-kappa B, pubmed-meshheading:15905464-Nitric Oxide, pubmed-meshheading:15905464-Nitric Oxide Synthase, pubmed-meshheading:15905464-Nitric Oxide Synthase Type III, pubmed-meshheading:15905464-RNA, Messenger, pubmed-meshheading:15905464-Reactive Oxygen Species
pubmed:year
2005
pubmed:articleTitle
Effects of recombinant adenovirus-mediated uncoupling protein 2 overexpression on endothelial function and apoptosis.
pubmed:affiliation
University of Ulsan College of Medicine, Seoul, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't