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阿尔茨海默病小鼠模型中松果体的转录组分析

Transcriptome Analysis of Pineal Glands in the Mouse Model of Alzheimer's Disease.

作者信息

Nam Kwang Il, Yoon Gwangho, Kim Young-Kook, Song Juhyun

机构信息

Department of Anatomy, Chonnam National University Medical School, Jeollanam-do, South Korea.

Department of Biochemistry, Chonnam National University Medical School, Jeollanam-do, South Korea.

出版信息

Front Mol Neurosci. 2020 Jan 9;12:318. doi: 10.3389/fnmol.2019.00318. eCollection 2019.

DOI:10.3389/fnmol.2019.00318
PMID:31998073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6962250/
Abstract

The pineal gland maintains the circadian rhythm in the body by secreting the hormone melatonin. Alzheimer's disease (AD) is the most common neurodegenerative disease. Pineal gland impairment in AD is widely observed, but no study to date has analyzed the transcriptome in the pineal glands of AD. To establish resources for the study on pineal gland dysfunction in AD, we performed a transcriptome analysis of the pineal glands of AD model mice and compared them to those of wild type mice. We identified the global change of diverse protein-coding RNAs, which are implicated in the alteration in cellular transport, protein transport, protein folding, collagen expression, histone dosage, and the electron transfer system. We also discovered various dysregulated long noncoding RNAs and circular RNAs in the pineal glands of mice with AD. This study showed that the expression of diverse RNAs with important functional implications in AD was changed in the pineal gland of the AD mouse model. The analyzed data reported in this study will be an important resource for future studies to elucidate the altered physiology of the pineal gland in AD.

摘要

松果体通过分泌褪黑素维持身体的昼夜节律。阿尔茨海默病(AD)是最常见的神经退行性疾病。AD患者中广泛观察到松果体功能受损,但迄今为止尚无研究分析AD患者松果体的转录组。为了建立AD松果体功能障碍研究的资源,我们对AD模型小鼠的松果体进行了转录组分析,并与野生型小鼠进行了比较。我们确定了多种蛋白质编码RNA的整体变化,这些变化与细胞转运、蛋白质转运、蛋白质折叠、胶原蛋白表达、组蛋白剂量和电子传递系统的改变有关。我们还在AD小鼠的松果体中发现了各种失调的长链非编码RNA和环状RNA。本研究表明,在AD小鼠模型的松果体中,具有重要功能意义的多种RNA的表达发生了变化。本研究报告的分析数据将成为未来阐明AD患者松果体生理改变的重要资源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/4270cb5d6a42/fnmol-12-00318-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/b182cfe41741/fnmol-12-00318-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/fab1e7c7c06e/fnmol-12-00318-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/8d668a6f719b/fnmol-12-00318-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/4270cb5d6a42/fnmol-12-00318-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/b182cfe41741/fnmol-12-00318-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/fab1e7c7c06e/fnmol-12-00318-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/8d668a6f719b/fnmol-12-00318-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3594/6962250/4270cb5d6a42/fnmol-12-00318-g0004.jpg

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Front Genet. 2019 Feb 19;10:83. doi: 10.3389/fgene.2019.00083. eCollection 2019.
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The transmembrane collagen COL-99 guides longitudinally extending axons in C. elegans.
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