Adiponectin enhances biological functions of vascular endothelial progenitor cells through the mTOR-STAT3 signaling pathway
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
29750888
DOI
10.33549/physiolres.933738
PII: 933738
Knihovny.cz E-resources
- MeSH
- Adiponectin pharmacology MeSH
- Cell Line MeSH
- Endothelium, Vascular drug effects metabolism MeSH
- Endothelial Progenitor Cells drug effects physiology MeSH
- Rats MeSH
- Cell Proliferation drug effects physiology MeSH
- Signal Transduction drug effects physiology MeSH
- Sulfones pharmacology MeSH
- TOR Serine-Threonine Kinases antagonists & inhibitors biosynthesis MeSH
- STAT3 Transcription Factor antagonists & inhibitors biosynthesis MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Adiponectin MeSH
- mTOR protein, rat MeSH Browser
- Stat3 protein, rat MeSH Browser
- Sulfones MeSH
- TOR Serine-Threonine Kinases MeSH
- STAT3 Transcription Factor MeSH
- XL388 MeSH Browser
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.
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