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Effect of chemokine-8 factor on the migration ability of human adipose derived mesenchymal stem cell in high glucose environment
ZHANG Peng ZHANG Xiao-dong JIANG Yang SUN Shi-zhu ZHANG Shan-qiang SHEN Lei*
Acta Anatomica Sinica ›› 2015, Vol. 46 ›› Issue (6) : 764-771.
Effect of chemokine-8 factor on the migration ability of human adipose derived mesenchymal stem cell in high glucose environment
Objective To investigate the effect of chemokines (CXCL)-8 factor on the chemotaxis ability of human adipose-derived mesenchymal stem cells (hADMSCs).
Methods The animals under the high glucose environment were divided into CXCL-8 experimental group, Akt inhibitor group and control group of high glucose. The normal control group was the cultural hADMSCs under the normal condition. Cell scratch, Transwells cell chamber experiment were used to check the effect of chemotaxis ability of CXCL-8 on the ADMSCs Western blotting, and ELISA experiment to check the protein expression of Akt, signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor (VEGF). Results Compared with the control group, the closing rate of hADMSCs cell scratch area in CXCL-8 experimental group and migration rate of Transwell cell chamber were increased (P＜0.01). The closing rate of cell scratch area in Akt inhibitor group and migration rate were decreased (P＜0.01). The protein expressions of phosphorylated Akt, mTOP and STAT3 were increased. The VEGF, epidermal growth factor (EGF) of liquid supernatant in CXCL-8 experimental group were increased significantly (P＜0.01); but the secretion ability of Akt inhibitor group was decreased (P＜0.01). Conclusion Under the high glucose environment, the CXCL-8 promoted MSCs paracrine VEGF factors through Akt-STAT3 pathway and promoted migration of MSCs, which may have the important meaning for recruit host cell homing and promote damage repair.
Chemokines-8 / Adipose-derived mesenchymal stem cell / High glucose environment / Paracrine / Homing / Human
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This study was supported by the Foundation of Department
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