Source:http://linkedlifedata.com/resource/pubmed/id/18633188
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2008-7-17
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| pubmed:abstractText |
We investigated whether a peroxisome proliferator-activated receptor (PPAR) agonist would effect the angiotensin II (Ang II)-induced senescence of endothelial progenitor cells (EPCs). EPCs were isolated from peripheral blood and characterized. Both reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to assess gp91phox expression and angiotensin type 1 receptor (AT1R) levels. Immunofluorescence of nitrotyrosine provided evidence of peroxynitrite formation. Our data indicate that Ang II increased the expression of gp91phox mRNA, which was significantly diminished by pioglitazone, a PPARgamma agonist. Western blotting revealed that Ang II stimulated an increase in the gp91phox protein, whereas co-treatment with pioglitazone significantly reduced this increase. In addition, pioglitazone also inhibited Ang II-induced peroxynitrite formation. Interestingly, pioglitazone decreased the expressions of AT1R mRNA and protein. The exposure of cultured EPCs to Ang II (100 nmol/L) significantly accelerated the rate of senescence compared to that of the control cells during 14 d in culture, as determined by acidic beta-galactosidase staining. Ang II-induced EPC senescence was significantly inhibited by co-treatment with pioglitazone. Because cellular senescence is critically influenced by telomerase, which elongates telomeres, we also measured telomerase activity by means of PCR-ELISA-based assay. The results showed that Ang II significantly diminished telomerase activity, and this effect was significantly abolished by co-treatment with pioglitazone. In conclusion, pioglitazone inhibited Ang II-induced senescence of EPCs via down-regulation of the expression of AT1R.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/CYBB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxynitrous Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/Telomerase,
http://linkedlifedata.com/resource/pubmed/chemical/Thiazolidinediones,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents,
http://linkedlifedata.com/resource/pubmed/chemical/pioglitazone
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0916-9636
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
31
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
757-65
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| pubmed:meshHeading |
pubmed-meshheading:18633188-Angiotensin II,
pubmed-meshheading:18633188-Cell Aging,
pubmed-meshheading:18633188-Cells, Cultured,
pubmed-meshheading:18633188-Drug Interactions,
pubmed-meshheading:18633188-Gene Expression,
pubmed-meshheading:18633188-Hematopoietic Stem Cells,
pubmed-meshheading:18633188-Humans,
pubmed-meshheading:18633188-Hypertension,
pubmed-meshheading:18633188-Hypoglycemic Agents,
pubmed-meshheading:18633188-Membrane Glycoproteins,
pubmed-meshheading:18633188-NADPH Oxidase,
pubmed-meshheading:18633188-Oxidative Stress,
pubmed-meshheading:18633188-Peroxynitrous Acid,
pubmed-meshheading:18633188-Receptor, Angiotensin, Type 1,
pubmed-meshheading:18633188-Superoxides,
pubmed-meshheading:18633188-Telomerase,
pubmed-meshheading:18633188-Thiazolidinediones,
pubmed-meshheading:18633188-Vasoconstrictor Agents
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| pubmed:year |
2008
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| pubmed:articleTitle |
Pioglitazone inhibits angiotensin II-induced senescence of endothelial progenitor cell.
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| pubmed:affiliation |
Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan. t-imani@wakayama-med.ac.jp
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| pubmed:publicationType |
Journal Article
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