Linked Life Data

15680482

Source:http://linkedlifedata.com/resource/pubmed/id/15680482

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2005-1-31
pubmed:abstractText
Oxidative stress is known to be involved in growth control of vascular smooth muscle cells (VSMCs). We and others have demonstrated that angiotensin II (Ang II) has an important role in vascular remodeling. Several reports suggested that VSMC growth induced by Ang II was elicited by oxidative stress. Gax, growth arrest-specific homeobox is a homeobox gene expressed in the cardiovascular system. Over expression of Gax is demonstrated to inhibit VSMC growth. We previously reported that Ang II down-regulated Gax expression. To address the regulatory mechanism of Gax, we investigated the significance of oxidative stress in Ang II-induced suppression of Gax expression. We further examined the involvement of mitogen-activated protein kinases (MAPKs), which is crucial for cell growth and has shown to be activated by oxidative stress, on the regulation of Gax expression by Ang II. Ang II markedly augmented intracellular H2O2 production which was decreased by pretreatment with N-acetylcystein (NAC), an anti-oxidant. Ang II and H2O2 decreased Gax expression dose-dependently and these effects were blocked by administration of both NAC and pyrrolidine dithiocarbamate (PDTC), another anti-oxidant. Ang II and H2O2 induced marked activation of extracellular signal-responsive kinase1/2 (ERK1/2), which was blocked by NAC. Ang II and H2O2 also activated p38MAPK, and they were blocked by pre-treatment with NAC. However, the level of activated p38MAPK was quite low in comparison with ERK1/2. Ang II- or H2O2 -induced Gax down-regulation was significantly inhibited by PD98059, an ERK1/2 inhibitor but not SB203580, a p38MAPK inhibitor. The present results demonstrated the significance of regulation of Gax expression by redox-sensitive ERK1/2 activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0167-0115
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
127
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-67
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15680482-Angiotensin II, pubmed-meshheading:15680482-Animals, pubmed-meshheading:15680482-Cells, Cultured, pubmed-meshheading:15680482-Enzyme Activation, pubmed-meshheading:15680482-Gene Expression Regulation, pubmed-meshheading:15680482-Homeodomain Proteins, pubmed-meshheading:15680482-Humans, pubmed-meshheading:15680482-Hydrogen Peroxide, pubmed-meshheading:15680482-Mitogen-Activated Protein Kinases, pubmed-meshheading:15680482-Muscle, Smooth, Vascular, pubmed-meshheading:15680482-Muscle Proteins, pubmed-meshheading:15680482-Myocytes, Smooth Muscle, pubmed-meshheading:15680482-Oxidants, pubmed-meshheading:15680482-Oxidation-Reduction, pubmed-meshheading:15680482-Oxidative Stress, pubmed-meshheading:15680482-Phosphorylation, pubmed-meshheading:15680482-RNA, Messenger, pubmed-meshheading:15680482-Rats, pubmed-meshheading:15680482-Reactive Oxygen Species
pubmed:year
2005
pubmed:articleTitle
Angiotensin II suppresses growth arrest specific homeobox (Gax) expression via redox-sensitive mitogen-activated protein kinase (MAPK).
pubmed:affiliation
Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't