Advanced Glycation End Products Promotes Apoptosis of Human Mesenchymal Stem Cells Through Oxidative Stress
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    Abstract:

    Aim To investigate the effects of advanced glycation end products(AGE-BSA) on oxidative stress and apoptosis in human bone marrow derived Mesenchymal stem cells(hMSC),providing new evidences for a higher survival of donor MSC in the heart of diabetes cardiomyopathy after clinical stem cell transplantation.Methods The adult hMSC were isolated from adult bone marrow and cultured in L-DMEM with 10%FCS,were suspended by trypsin and passaged for subsequent passages.At the third passage,hMSC were identified as the immunophenotype of cell surface CD44,CD105,CD34 on flow cytometry.Then,hMSC were cultured in the absence or presence of AGE-BSA for 24 hours.CCK8 were used to evaluate the proliferation capability,reactivated oxygen species(ROS) were analyzed using the ROS assay kit,the content of malondialdehyde(MDA),the activity of superoxide dismutase(SOD) were measured;the cell apotosis was detected by Annexin V/PI flow cytometry.Results The hMSC exhibited adherent long spindle-shaped cells.The immunophenotype of hMSC showed that both stromal cell-associated markers(CD44) and the stem cell-associated marker(CD105) were positive,which were 97.8% and 98.9%,while blood cell,endothelial cell-associated marker(CD34) was negative,which was only 0.8%.Compared with the control group,co-culturing with 20,50,100,200 mg/L AGE-BSA increased ROS production,the content of MDA in cells and the rate of apoptosis.Simultaneously,AGEBSA decreased antioxidase and proliferation of the cells.Both of them were in a dose dependent manner.Conclusion AGE increases the production of ROS in hMSC,while weakens the production of antioxidases,it increases the oxidative stress,breaks the homeostasis of cells,accordingly,AGE inhibits the proliferation of hMSC and increases the apoptosis of these cells.

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LIU Zhao, BIAN Yun-Fei, and XIAO Chuan-Shi. Advanced Glycation End Products Promotes Apoptosis of Human Mesenchymal Stem Cells Through Oxidative Stress[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2011,19(5):399-404.

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  • Received:January 24,2011
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