Advanced glycation end products inhibit neural stem cell differentiation via upregualtion of HDAC3 expression.

Yi Bao, Haiyan Chen, Zheng Cai, Jiaoyang Zheng, Junjie Zou, Yongquan Shi, Lei Jiang

Brain research bulletin 2020 Jun

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Diabetes mellitus (DM) is a highly prevalent chronic systemic disease, which may cause cognitive decline and degenerative change of the brain. Neuronal differentiation defects of neural stem cells (NSCs) played an important role in the development and progression of diabetes-associated cognitive decline (DACD), but the intrinsic pathological mechanism remains largely unclear. In the present study, we demonstrated that expression level of HDAC3 was upregulated in diabetic mice with reduced learning and memory abilities and in cultured NSCs after advanced glycation end products (AGEs) induction. In addition, AGEs interfered with normal differentiation of the cultured NSCs, and knocking down the expression of HDAC3 could partially attenuate the inhibitory effect of AGEs on NSCs differentiation. Findings in this study demonstrate that HDAC3 may serve as an experimental clue for revealing the pathogenesis of DACD. Copyright © 2020. Published by Elsevier Inc.

Citation

Yi Bao, Haiyan Chen, Zheng Cai, Jiaoyang Zheng, Junjie Zou, Yongquan Shi, Lei Jiang. Advanced glycation end products inhibit neural stem cell differentiation via upregualtion of HDAC3 expression. Brain research bulletin. 2020 Jun;159:1-8