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http://dx.doi.org/10.14348/molcells.2016.2159

Human Amnion-Derived Mesenchymal Stem Cells Protect Human Bone Marrow Mesenchymal Stem Cells against Oxidative Stress-Mediated Dysfunction via ERK1/2 MAPK Signaling  

Wang, Yuli (Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University)
Ma, Junchi (Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University)
Du, Yifei (Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University)
Miao, Jing (Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University)
Chen, Ning (Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University)
Abstract
Epidemiological evidence suggests that bone is especially sensitive to oxidative stress, causing bone loss in the elderly. Previous studies indicated that human amnion-derived mesenchymal stem cells (HAMSCs), obtained from human amniotic membranes, exerted osteoprotective effects in vivo. However, the potential of HAMSCs as seed cells against oxidative stress-mediated dysfunction is unknown. In this study, we systemically investigated their antioxidative and osteogenic effects in vitro. Here, we demonstrated that HAMSCs significantly promoted the proliferation and osteoblastic differentiation of $H_2O_2$-induced human bone marrow mesenchymal stem cells (HBMSCs), and down-regulated the reactive oxygen species (ROS) level. Further, our results suggest that activation of the ERK1/2 MAPK signal transduction pathway is essential for both HAMSCs-mediated osteogenic and protective effects against oxidative stress-induced dysfunction in HBMSCs. U0126, a highly selective inhibitor of extracellular ERK1/2 MAPK signaling, significantly suppressed the antioxidative and osteogenic effects in HAMSCs. In conclusion, by modulating HBMSCs, HAMSCs show a strong potential in treating oxidative stress- mediated bone deficiency.
Keywords
ERK1/2 MAPK signal transduction pathway; human amnion mesenchymal stem cells (HAMSCs); human bone marrow mesenchymal stem cells (HBMSCs); oxidative stress; reactive oxygen species (ROS);
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