Adiponectin enhances biological functions of vascular endothelial progenitor cells through the mTOR-STAT3 signaling pathway

Title:

Adiponectin enhances biological functions of vascular endothelial progenitor cells through the mTOR-STAT3 signaling pathway

Creator:

Dong, Xiaoying, Yan, Xia, Zhang, Wei, and Tang, Shengqiu

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0a6dae70-9452-440a-b8b7-81f6ebb9dab0
uuid:0a6dae70-9452-440a-b8b7-81f6ebb9dab0
issn:0862-8408

Subject:

apoptóza, apoptosis, adiponectin, VEPCs, proliferation, mTOR, STAT3, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

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., Xiaoying Dong, Xia Yan, Wei Zhang, Shengqiu Tang., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:4

Harvested from:

CDK

Metadata only:

false