Abstract
Objective to explore the effects of Hyperglycemia and AGEs on human ADSCs’ osteogenesis ability. Methods Human adipose derived stromal cells were isolated and induce to the bone formation; 27.5 mmol/L high glucose concentration and 100μg/ml AGEs were used to simulate the diabetic environment. There were four groups in the present study, 6 specimen in each group. Through immunofluorescence detection and observation of calcification in each group, the different change in CNI secretion and osteogeniesis ability were statistically analyzed. Results Hyperglycemia and AGEs prevented ADSCs cognate differentiation into bone. On 21d, the CNI amount in combination group was 2.76 time lower than the normal group, and the average calcification nodes was (4.10±1.24).There were significant difference in these two groups (P<0.01) Conclusion Hyperglycemia and AGEs had a deleterious effect on ADSCs’ osteogenesis ability.
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References
Christopher, J.: Trabecular microfracture and the influence of pyridinium and non-enzymatic glycation mediated collagen cross-links. J. Bone 37(6), 825–832 (2005)
Valcour, U.: Non-enzymatic Glycation of Bone Collagen Modifies Osteoclastic Activity and Differentiation. Journal of Biological Chemistry 282(8), 5691–5703 (2007)
Zuk, P.A., Zhu, M., Mizuno, H., et al.: Multilineage cells form human adipose tissue: implications for cell-based therapies. Tissue Eng. 7, 211–228 (2001)
Hong, L., Peptan, I.A., Colpan, A., et al.: Adipose tissue engineering by human adipose-derived stroma cells. Cells Tissues Organs 183(3), 133–140 (2006)
Santana, R.B., Xu, L.: A role for advanced glycation end products in diminished bone healing in type 1 diabetes. Diabetes 52(6), 1502–1510 (2003)
Geoffroy, K., Wiernsperger, N., Lagarde, M., et al.: Bimodal effect of advanced glycation end production on mesangial cell proliferation if mediated by neutral ceramidase regulation and endogenous sphingolipids. J. Biol. Chem. 279, 34343–34352 (2004)
Chen, B.H., Jiang, D.Y., et al.: Advanced glycation end- products induce apoptosis involving the signaling pathways of oxidative stress in bovine retinal pericytes. Life Sci. 79(11), 1040–1048 (2006)
Shinichiro, K., Seiya, K., Yamagishi, S.-I., et al.: Advanced glycation end-products attenuate human mesenchymal stem cells and prevent cognate differentiation into adipose tissue, cartilage and bone. Journal of Bone and Mineral Research 20(9), 1647–1658 (2005)
Mamputu, J.C., Renier: Advanced glycation end products increase, through a protein kinase C-dependent pathway, vascular endothelial growth factor expression in retinal endothelialcells. Inhibitory effect of gliclazide. J. Diabetes Complications 16, 284–293 (2000)
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Song, L.D., Qiang, L.S., Bo, C., Ping, W., Wei, F., Guo, L.J. (2012). Hyperglycemia and Advanced Glycation End-Products Prevent Cognate Differentiation of Human Adipose- Derived Stromal Cells into Bone In Vitro. In: Zhu, E., Sambath, S. (eds) Information Technology and Agricultural Engineering. Advances in Intelligent and Soft Computing, vol 134. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-27537-1_16
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DOI: https://doi.org/10.1007/978-3-642-27537-1_16
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