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三丁基锡诱导培养大鼠中脑神经干细胞凋亡的转录组。

Transcriptome of tributyltin-induced apoptosis of the cultured rat mesencephalic neural stem cells.

机构信息

Center for Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan.

出版信息

Toxicology. 2011 Sep 5;287(1-3):61-8. doi: 10.1016/j.tox.2011.06.001. Epub 2011 Jun 13.

Abstract

Exposure to environmental neurotoxic chemicals both in utero and during the early postnatal period can cause neurodevelopmental disorders. To evaluate the disruption of neurodevelopmental programming, we previously established an in vitro neurosphere assay system, using rat mesencephalic neural stem cells (mNSC). Here, we examined the developmental neurotoxicity of tributyltin (TBT) in an in vitro neurosphere assay. A neurosphere was driven from rat E16 mesencephalon and seeded in a poly-l-ornithine/laminin-coated plate. Exposure to TBT increased the number of terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL)-positive cells in time-dependent and dose-dependent manner: it was significantly detectable with treatment of 100pM TBT for 90min, or of 1μM TBT for 30min. Disruption of mitochondrial membrane potential and activation of caspase-3/7 were concomitantly observed. Furthermore, DNA microarray analyses using Affymetrix GeneChip revealed that as early as 0.5h after exposure to the metal (1μM), the expression levels of 71 genes were increased by more than 2-fold, whereas those of 8 genes were decreased by 2-fold or less: it was notably altered in expression of Ca(2+)-mobilizing-related genes, and retinoic-acid signal-related genes, as well as bifunctional apoptosis-related genes. The levels of gene expression of Wnt family were also significantly changed. Thus, we established transcriptome of TBT-induced apoptosis of mNSC. This would help to evaluate developmental neurotoxicity of TBT in vivo, contributing to the risk assessment methods based on infant physiology.

摘要

暴露于环境神经毒性化学物质,无论是在子宫内还是在出生后的早期,都可能导致神经发育障碍。为了评估神经发育编程的中断,我们之前建立了一种体外神经球测定系统,使用大鼠中脑神经干细胞(mNSC)。在这里,我们在体外神经球测定中检查了三丁基锡(TBT)的发育神经毒性。从大鼠 E16 中脑驱动神经球,并接种在多聚-l-鸟氨酸/层粘连蛋白包被的平板上。TBT 的暴露以时间依赖性和剂量依赖性方式增加末端脱氧核苷酸转移酶(TdT)介导的 dUTP 缺口末端标记(TUNEL)阳性细胞的数量:用 100pM TBT 处理 90 分钟,或用 1μM TBT 处理 30 分钟,即可显著检测到。同时观察到线粒体膜电位的破坏和 caspase-3/7 的激活。此外,使用 Affymetrix GeneChip 的 DNA 微阵列分析显示,早在暴露于金属(1μM)后的 0.5 小时,71 个基因的表达水平增加了 2 倍以上,而 8 个基因的表达水平降低了 2 倍或更低:钙(Ca2+)动员相关基因、视黄酸信号相关基因以及双功能凋亡相关基因的表达明显改变。Wnt 家族的基因表达水平也发生了显著变化。因此,我们建立了 TBT 诱导的 mNSC 凋亡的转录组。这将有助于评估 TBT 在体内的发育神经毒性,为基于婴儿生理学的风险评估方法做出贡献。

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