Thyroid Hormone Enhances Neurite Outgrowth in Neuroscreen 1 Cells.

Thyroid Hormone Enhances Neurite Outgrowth in Neuroscreen 1 Cells.
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DOI:
10.31531/2581-4745.1000104
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发表时间:
2018-01-01
期刊:
International journal of biomedical investigation
影响因子:
--
通讯作者:
D, Lopez
D, Lopez
中科院分区:
其他
文献类型:
--
作者:
Ce, Oldham;Cj, Wooten;D, Lopez

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阿尔茨海默病(AD)是一种神经退行性疾病,影响数百万人。此外,甲状腺功能减退症已被确定为可能导致AD发展的危险因素之一。在这里,我们调查是否有一个相关性蛋白质的表达水平参与形成AD病变,神经突生长,甲状腺激素level.METHODS:细胞生长在培养基中补充不同水平的3,5,3 '-三碘甲状腺原氨酸(T3),然后处理神经突生长和制备RNA样品。使用定量实时PCR分析RNA样品。蛋白质水平测定使用在cell-Western blotting analysis.RESULTS:通过使用神经突起生长的研究,它表明,T3处理增强神经突起生长在NS-1细胞中的时间和剂量依赖性的方式。定量实时PCR研究进一步证实,NS-1细胞表达大量的TR α和显著较少的TR β,这两者都可能是T3依赖性影响神经突生长的原因。虽然整体tau蛋白的表达没有受到影响,在响应T3治疗,剪接的tau外显子10的方向产生更多的tau分子,排除外显子(tau 3R)的影响。结论:这项研究的结果是至关重要的,不仅要了解甲状腺功能减退症和AD之间的可能联系,但也为未来的预防和治疗甲状腺功能减退症患者的AD提供了依据。
OBJECTIVES: Alzheimer's disease (AD) is a neurodegenerative disorder that affects millions of individuals. Moreover, hypothyroidism has been identified as one of the risk factors that may contribute to the development of AD. Here, we investigated whether there was a correlation among expression levels of proteins involved in the formation of AD lesions, neurite outgrowth, and thyroid hormone levels.METHODS: Cells were grown in media supplemented with different levels of 3,5,3'-triiodothyronine (T3) and then processed for neurite outgrowth and to prepare RNA samples. RNA samples were analysed using quantitative real-time PCR. Protein levels were measured using in cell-Western blotting analysis.RESULTS: By using neurite outgrowth studies, it was demonstrated that T3 treatment enhanced neurite outgrowth in NS-1 cells in a time- and dose-dependent manner. Quantitative real-time PCR studies further confirmed that NS-1 cells expressed substantial levels of TRalpha and significantly less TRbeta, either of which could be responsible for the T3-dependent effects on neurite outgrowth. Although the overall tau protein expression was not affected in response to T3 treatment, the splicing of tau exon 10 was impacted in the direction of producing more tau molecules that excluded the exon (tau 3R).CONCLUSION: The results of this study are critical not only to understand the probable link between hypothyroidism and AD but also in providing the basis for future prevention and treatment of AD in hypothyroid patients.