Regulation of proapoptotic proteins Bak1 and p53 by miR-125b in an experimental model of Alzheimer's disease: Protective role of 17β-estradiol

被引：28

作者：

Micheli, F. ^{[1
]}

Palermo, R. ^{[3
]}

Talora, C. ^{[1
]}

Ferretti, E. ^{[2
]}

Vacca, A. ^{[2
]}

Napolitano, M. ^{[1
]}

机构：

[1] Univ Roma La Sapienza, Dept Mol Med, I-00161 Rome, Italy

[2] Univ Roma La Sapienza, Dept Expt Med, Rome, Italy

[3] Ist Italiano Tecnol, Ctr Life Nano Sci Sapienza, Rome, Italy

来源：

NEUROSCIENCE LETTERS | 2016年 / 629卷

关键词：

Alzheimer' disease; mir-125b; 17; beta-Estradiol; PEPTIDE-INDUCED NEUROTOXICITY; CULTURED CORTICAL-NEURONS; CANCER CELLS; EXPRESSION; MICRORNAS; BCL-2; STABILITY; APOPTOSIS; LEUKEMIA;

D O I：

10.1016/j.neulet.2016.05.049

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease has become one of the most impacting disorders since world population is rapidly aging. MicroRNA-125b plays a crucial role in many cellular processes and pathologies, but, to date, its role in Alzheimer's disease is controversial. In this study, we demonstrated, for the first time, that the down regulation of miR-125b is a key event for the neurotoxic effect of A beta treatment in cortical neurons. Moreover, we found that 17 beta-estradiol treatment protects neurons from the A beta-peptide induced neurotoxicity by increasing miR-125b expression that, in turn, decreased the expression, both at gene and protein levels, of the pro-apoptopic proteins Bak1 and p53. Overall, our data reveal miR-125b as a novel neuro-protector miRNA in Alzheimer's disease. (C) 2016 Published by Elsevier Ireland Ltd.

引用

页码：234 / 240

页数：7

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