Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.

<h4>Background</h4>A large number of studies have confirmed that excessive apoptosis is one of the reasons for deficient neuronal function in neural tube defects (NTDs). A previous study from our laboratory used 2-D gel electrophoresis to demonstrate that 14-3-3ζ expression was low in th...

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Autores principales: Li-na Wu, Xiao-wei Wei, Yang Fan, Jia-ning Miao, Li-li Wang, Yi Zhang, Di Wu, Zheng-wei Yuan
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spelling oai:doaj.org-article:064ae31107ac49ea90385131f145649d2021-11-18T09:01:00ZAltered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.1932-620310.1371/journal.pone.0070457https://doaj.org/article/064ae31107ac49ea90385131f145649d2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23936434/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>A large number of studies have confirmed that excessive apoptosis is one of the reasons for deficient neuronal function in neural tube defects (NTDs). A previous study from our laboratory used 2-D gel electrophoresis to demonstrate that 14-3-3ζ expression was low in the spinal cords of rat fetuses with spina bifida aperta at embryonic day (E) 17. As a member of the 14-3-3 protein family, 14-3-3ζ plays a crucial role in the determination of cell fate and anti-apoptotic activity. However, neither the expression of 14-3-3ζ in defective spinal cords, nor the correlation between 14-3-3ζ and excessive apoptosis in NTDs has been fully confirmed.<h4>Methodology/principal findings</h4>We used immunoblotting and quantitative real-time PCR (qRT-PCR) to quantify the expression of 14-3-3ζ and double immunofluorescence to visualize 14-3-3ζ and apoptosis. We found that, compared with controls, 14-3-3ζ was down-regulated in spina bifida between E12 and E15. Excessive apoptotic cells and low expression of 14-3-3ζ were observed in the dorsal region of spinal cords with spina bifida during the same time period. To initially explore the molecular mechanisms of apoptosis in NTDs, we investigated the expression of microRNA-7 (miR-7), microRNA-375 (miR-375) and microRNA-451 (miR-451), which are known to down-regulate 14-3-3ζ in several different cell types. We also investigated the expression of p53, a molecule that is downstream of 14-3-3ζ and can be down-regulated by it. We discovered that, in contrast to the reduction of 14-3-3ζ expression, the expression of miR-451, miR-375 and p53 increased in spina bifida rat fetuses.<h4>Conclusions/significance</h4>These data suggest that the reduced expression of 14-3-3ζ plays a role in the excessive apoptosis that occurs in spina bifida and may be partly regulated by the over-expression of miR-451 and miR-375, and the consequent up-regulation of p53 might further promote apoptosis in spina bifida.Li-na WuXiao-wei WeiYang FanJia-ning MiaoLi-li WangYi ZhangDi WuZheng-wei YuanPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e70457 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Li-na Wu
Xiao-wei Wei
Yang Fan
Jia-ning Miao
Li-li Wang
Yi Zhang
Di Wu
Zheng-wei Yuan
Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
description <h4>Background</h4>A large number of studies have confirmed that excessive apoptosis is one of the reasons for deficient neuronal function in neural tube defects (NTDs). A previous study from our laboratory used 2-D gel electrophoresis to demonstrate that 14-3-3ζ expression was low in the spinal cords of rat fetuses with spina bifida aperta at embryonic day (E) 17. As a member of the 14-3-3 protein family, 14-3-3ζ plays a crucial role in the determination of cell fate and anti-apoptotic activity. However, neither the expression of 14-3-3ζ in defective spinal cords, nor the correlation between 14-3-3ζ and excessive apoptosis in NTDs has been fully confirmed.<h4>Methodology/principal findings</h4>We used immunoblotting and quantitative real-time PCR (qRT-PCR) to quantify the expression of 14-3-3ζ and double immunofluorescence to visualize 14-3-3ζ and apoptosis. We found that, compared with controls, 14-3-3ζ was down-regulated in spina bifida between E12 and E15. Excessive apoptotic cells and low expression of 14-3-3ζ were observed in the dorsal region of spinal cords with spina bifida during the same time period. To initially explore the molecular mechanisms of apoptosis in NTDs, we investigated the expression of microRNA-7 (miR-7), microRNA-375 (miR-375) and microRNA-451 (miR-451), which are known to down-regulate 14-3-3ζ in several different cell types. We also investigated the expression of p53, a molecule that is downstream of 14-3-3ζ and can be down-regulated by it. We discovered that, in contrast to the reduction of 14-3-3ζ expression, the expression of miR-451, miR-375 and p53 increased in spina bifida rat fetuses.<h4>Conclusions/significance</h4>These data suggest that the reduced expression of 14-3-3ζ plays a role in the excessive apoptosis that occurs in spina bifida and may be partly regulated by the over-expression of miR-451 and miR-375, and the consequent up-regulation of p53 might further promote apoptosis in spina bifida.
format article
author Li-na Wu
Xiao-wei Wei
Yang Fan
Jia-ning Miao
Li-li Wang
Yi Zhang
Di Wu
Zheng-wei Yuan
author_facet Li-na Wu
Xiao-wei Wei
Yang Fan
Jia-ning Miao
Li-li Wang
Yi Zhang
Di Wu
Zheng-wei Yuan
author_sort Li-na Wu
title Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
title_short Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
title_full Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
title_fullStr Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
title_full_unstemmed Altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
title_sort altered expression of 14-3-3ζ protein in spinal cords of rat fetuses with spina bifida aperta.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/064ae31107ac49ea90385131f145649d
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