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雄性急性和慢性睡眠剥夺小鼠食管组织的差异表达基因

Differentially expressed genes of esophageal tissue in male acute and chronic sleep deprivation mice.

作者信息

Li Jing, Lu Yifan, Yang Dingding, Ren Mudan, Yin Yan, Zhao Yan, He Shuixiang

机构信息

Department of Gastroenterology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Shannxi Clinical Research Center of Digestive Disease (Cancer Devision), Xi'an, China.

出版信息

Genes Brain Behav. 2024 Apr;23(2):e12896. doi: 10.1111/gbb.12896.

DOI:10.1111/gbb.12896
PMID:38662955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11045192/
Abstract

Gastroesophageal reflux disease (GERD) is associated with sleep disturbances. However, mechanisms underlying these interactions remain unclear. Male acute and chronic sleep deprivation (SD) mice were used for this study. Mice in the chronic SD group exhibited anxiety- and depression-like behaviors. We further performed high-throughput genome sequencing and bioinformatics analysis to screen for featured differentially expressed genes (DEGs) in the esophageal tissue. The acute SD group, comprised 25 DEGs including 14 downregulated and 11 upregulated genes. Compared with the acute SD group, more DEGs were present in the chronic SD group, with a total of 169 DEGs, including 88 downregulated and 81 upregulated genes. Some DEGs that were closely related to GERD and associated esophageal diseases were significantly different in the chronic SD group. Quantitative real-time polymerase chain reaction verified the downregulation of Krt4, Krt13, Krt15 and Calml3 and upregulation of Baxl1 and Per3. Notably, these DEGs are involved in biological processes, which might be the pathways of the neuroregulatory mechanisms of DEGs expression.

摘要

胃食管反流病(GERD)与睡眠障碍有关。然而,这些相互作用背后的机制仍不清楚。本研究使用雄性急性和慢性睡眠剥夺(SD)小鼠。慢性SD组小鼠表现出焦虑和抑郁样行为。我们进一步进行了高通量基因组测序和生物信息学分析,以筛选食管组织中有特征的差异表达基因(DEG)。急性SD组包括25个DEG,其中14个基因下调,11个基因上调。与急性SD组相比,慢性SD组中存在更多的DEG,共有169个DEG,其中88个基因下调,81个基因上调。一些与GERD和相关食管疾病密切相关的DEG在慢性SD组中有显著差异。定量实时聚合酶链反应验证了Krt4、Krt13、Krt15和Calml3的下调以及Baxl1和Per3的上调。值得注意的是,这些DEG参与生物过程,这可能是DEG表达的神经调节机制途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/7d357ca98ae8/GBB-23-e12896-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/412a129bd127/GBB-23-e12896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/b59528f30e7a/GBB-23-e12896-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/7dacbbf06dbe/GBB-23-e12896-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/6fde08395d5c/GBB-23-e12896-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/7d357ca98ae8/GBB-23-e12896-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/412a129bd127/GBB-23-e12896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/b59528f30e7a/GBB-23-e12896-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/7dacbbf06dbe/GBB-23-e12896-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/6fde08395d5c/GBB-23-e12896-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6acf/11045192/7d357ca98ae8/GBB-23-e12896-g005.jpg

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Front Public Health. 2022 Nov 15;10:1003361. doi: 10.3389/fpubh.2022.1003361. eCollection 2022.
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OTUB2 exerts tumor-suppressive roles via STAT1-mediated CALML3 activation and increased phosphatidylserine synthesis.OTUB2 通过 STAT1 介导的 CALML3 激活和增加磷脂酰丝氨酸合成发挥肿瘤抑制作用。
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Brain-wide mapping of c-Fos expression with fluorescence micro-optical sectioning tomography in a chronic sleep deprivation mouse model.
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Neurobiol Stress. 2022 Aug 7;20:100478. doi: 10.1016/j.ynstr.2022.100478. eCollection 2022 Sep.
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Comparative Analysis of Mutation Status and Immune Landscape for Squamous Cell Carcinomas at Different Anatomical sites.不同解剖部位鳞状细胞癌的突变状态和免疫景观的比较分析。
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