English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

Pioglitazone Inhibits Angiotensin II–Induced Senescence of Endothelial Progenitor Cell