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

被引：8

作者：

Bao, Yi ^{[1
]}

Chen, Haiyan ^{[1
]}

Cai, Zheng ^{[2
]}

Zheng, Jiaoyang ^{[1
]}

Zou, Junjie ^{[1
]}

Shi, Yongquan ^{[1
]}

Jiang, Lei ^{[2
]}

机构：

[1] Second Mil Med Univ, Changzheng Hosp, Dept Endocrinol, 415 Fengyang Rd, Shanghai 200003, Peoples R China

[2] Second Mil Med Univ, Changzheng Hosp, Dept Neurosurg, 415 Fengyang Rd, Shanghai 200003, Peoples R China

来源：

BRAIN RESEARCH BULLETIN | 2020年 / 159卷

基金：

中国国家自然科学基金;

关键词：

Diabetes mellitus; Neural stem cell; Advanced glycation end products; HDAC3; NEURONAL DIFFERENTIATION; MEDIATED ACTIVATION; ADULT NEUROGENESIS; PEPTIDE-1; RECEPTOR; PLASTICITY; DAMAGE;

D O I：

10.1016/j.brainresbull.2020.03.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：1 / 8

页数：8

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