Open Access

ARTICLE

Gene expression profile of Sox1, Sox2, p53, Bax and Nestin in neural stem cells and adult mouse brain tissues

by HAIFENG WANG, KAI WANG, JUAN GUO, TIEQIAO WEN

1 School of Environmental Engineering, Central Plains Specialty Food Engineering&Technology Research Center, Kaifeng Key Laboratory of Food Composition and Quality Assessment, Yellow River Conservancy Technical Institute, Dong Jing Avenue, Kaifeng, 475004, China
2 Laboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, 99 Shang Da Road, Shanghai, 200444, China

* Address correspondence to: Tieqiao Wen,

BIOCELL 2019, 43(2), 59-64. https://doi.org/10.32604/biocell.2019.05731

Abstract

Histone deacetylation is a key modulator involved in cell proliferation, apoptosis, and mRNA transcription. However, the effects of histone deacetylation on C17.2 neural stem cells (NSCs) remain unclear. Here, the histone deacetylase inhibitors nicotinamide and trichostatin A (TSA) were used to determine the role of histone deacetylation on gene transcription in NSCs. The results showed that the mRNA expression of p53, Sox1, Sox2, and Bax were significantly higher in E14.5 NSCs than in C17.2 NSCs. Nestin, a marker gene of neuronal differentiation, did not differ significantly between E14.5 NSCs and C17.2 NSCs. The transcription levels of p53 and Nestin were significantly higher in C17.2 NSCs than in differentiated brain tissues, and the expression of Bax, Sox1, and Sox2 was higher in the olfactory bulb than in other brain tissues. Nicotinamide and TSA treatment decreased the transcription of Sox2, p53, Nestin, and Bax in C17.2 NSCs, although the difference was statistically significant only for Sox2 and Nestin, Sox1 transcription was not detected. These results demonstrated that mRNA expression profiles differ between C17.2 NSCs, E14.5 NSCs, and adult mouse brain tissues, and HDAC inhibitors regulate gene expression by modulating histone acetylation.

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Keywords

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