Adiponectin mediates endothelial progenitor cell proliferation through mTOR-STAT3 signaling pathway

作者：Jiang, Shujun; Yang, Hong; Liu, Zhonghui; Wang, Huaixin^*

来源：International Journal of Clinical and Experimental Pathology, 2016, 9(2): 2738-2743.

• Adiponectin
• mTOR
• STAT3
• endothelial progenitor cell

Adiponectin and endothelial progenitor cells (EPCs) were both related to cardiovascular disease. Patients with cardiovascular disease are characterized by hypoadiponectinemia and EPCs number decrease in the circulation. Adiponectin is correlated with EPCs. It was found that adiponectin can promote EPCs proliferation, whereas mTOR/STAT3 signaling pathway is closely associated with cell proliferation, differentiation, and apoptosis. Thus, this study aimed to clarify the role of mTOR/STAT3 signaling pathway in adiponectin promoting EPCs proliferation by culturing EPCs in umbilical cord blood and detecting p-mTOR and p-STAT3 protein level. Ficoll density gradient centrifugation was applied to collect mononuclear cells from human umbilical cord blood. Flow cytometry was performed to identify cell phenotype after adherent culture screening. CCK8 was used to test cell proliferation, and Western blot was used to detect p-mTOR and p-STAT3 protein expression level. To further verify mTOR/STAT3 effect, the cells were divided into control, rapamycin group, adiponectin group, and rapamycin + adiponectin group. The cells proportion with CD34(+), CD133(+), CD31(+), and KDR+ positive surface markers were 68.12 +/- 7.68%, 18.65 +/- 4.24%, 5.42 +/- 6.43%, and 86.25 +/- 7.56%, respectively. Adiponectin may promote EPCs proliferation with time and dose dependent. P-mTOR and p-STAT3 protein level increased following adiponectin concentration. mTOR inhibitor rapamycin can suppress adiponectin induced EPCs proliferation. Rapamycin weakened adiponectin facilitating effect on p-mTOR and p-STAT3 protein expression in EPCs. Adiponectin can regulate EPCs proliferation through mTOR/STAT3 signaling pathway.

• 出版日期2016
• 单位潍坊医学院