Adiponectin enhances biological functions of vascular endothelial progenitor cells through the mTOR-STAT3 signaling pathway
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
29750888
DOI
10.33549/physiolres.933738
PII: 933738
Knihovny.cz E-zdroje
- MeSH
- adiponektin farmakologie MeSH
- buněčné linie MeSH
- cévní endotel účinky léků metabolismus MeSH
- endoteliální progenitorové buňky účinky léků fyziologie MeSH
- krysa rodu Rattus MeSH
- proliferace buněk účinky léků fyziologie MeSH
- signální transdukce účinky léků fyziologie MeSH
- sulfony farmakologie MeSH
- TOR serin-threoninkinasy antagonisté a inhibitory biosyntéza MeSH
- transkripční faktor STAT3 antagonisté a inhibitory biosyntéza MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adiponektin MeSH
- mTOR protein, rat MeSH Prohlížeč
- Stat3 protein, rat MeSH Prohlížeč
- sulfony MeSH
- TOR serin-threoninkinasy MeSH
- transkripční faktor STAT3 MeSH
- XL388 MeSH Prohlížeč
Adiponectin (APN), an adipose tissue-excreted adipokine, plays protective roles in metabolic and cardiovascular diseases. In this study, the effects and mechanisms of APN on biological functions of rat vascular endothelial progenitor cells (VEPCs) were investigated in vitro. After administrating APN in rat VEPCs, the proliferation was measured by methyl thiazolyl tetrazolium (MTT) method, the apoptotic rate was test by Flow cytometry assay, mRNA expression of B-cell lymphoma-2 (Bcl-2) and vascular endothelial growth factor (VEGF) was determined by real-time reverse transcriptase polymerase chain reaction (RT-PCR), and protein expression of mechanistic target of rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 (pSTAT3) was analyzed by Western blot. It was suggested that APN promoted the optical density (OD) value of VEPCs, enhanced mRNA expression of Bcl-2 and VEGF, and inhibited cell apoptotic rate. Furthermore, protein expression of pSTAT3 was also increased in the presence of APN. Moreover, APN changed-proliferation, apoptosis and VEGF expression of VEPCs were partially suppressed after blocking the mTOR-STAT3 signaling pathway by the mTOR inhibitor XL388. It was indicated that APN promoted biological functions of VEPCs through targeting the mTOR-STAT3 signaling pathway.
Citace poskytuje Crossref.org