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来自雄性和雌性小鼠的GPER缺陷心肌细胞中的炎症和线粒体基因表达数据。

Inflammatory and mitochondrial gene expression data in GPER-deficient cardiomyocytes from male and female mice.

作者信息

Wang Hao, Sun Xuming, Chou Jeff, Lin Marina, Ferrario Carlos M, Zapata-Sudo Gisele, Groban Leanne

机构信息

Department of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA; Internal Medicine/Molecular Medicine, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA.

Department of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA.

出版信息

Data Brief. 2016 Nov 23;10:465-473. doi: 10.1016/j.dib.2016.11.057. eCollection 2017 Feb.

DOI:10.1016/j.dib.2016.11.057
PMID:28054009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5198850/
Abstract

We previously showed that cardiomyocyte-specific G protein-coupled estrogen receptor (GPER) gene deletion leads to sex-specific adverse effects on cardiac structure and function; alterations which may be due to distinct differences in mitochondrial and inflammatory processes between sexes. Here, we provide the results of Gene Set Enrichment Analysis (GSEA) based on the DNA microarray data from GPER-knockout versus GPER-intact (intact) cardiomyocytes. This article contains complete data on the mitochondrial and inflammatory response-related gene expression changes that were significant in GPER knockout versus intact cardiomyocytes from adult male and female mice. The data are supplemental to our original research article "Cardiomyocyte-specific deletion of the G protein-coupled estrogen receptor (GPER) leads to left ventricular dysfunction and adverse remodeling: a sex-specific gene profiling" (Wang et al., 2016) [1]. Data have been deposited to the Gene Expression Omnibus (GEO) database repository with the dataset identifier GSE86843.

摘要

我们之前表明,心肌细胞特异性G蛋白偶联雌激素受体(GPER)基因缺失会对心脏结构和功能产生性别特异性的不良影响;这些改变可能是由于两性之间线粒体和炎症过程存在明显差异所致。在此,我们基于来自GPER基因敲除型与GPER完整型(完整)心肌细胞的DNA微阵列数据,提供基因集富集分析(GSEA)的结果。本文包含了与线粒体和炎症反应相关的基因表达变化的完整数据,这些变化在成年雄性和雌性小鼠的GPER基因敲除型与完整型心肌细胞中具有显著性差异。这些数据是我们原始研究文章《心肌细胞特异性缺失G蛋白偶联雌激素受体(GPER)导致左心室功能障碍和不良重塑:性别特异性基因谱分析》(Wang等人,2016年)[1]的补充资料。数据已存入基因表达综合数据库(GEO),数据集标识符为GSE86843。

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本文引用的文献

1
Cardiomyocyte-specific deletion of the G protein-coupled estrogen receptor (GPER) leads to left ventricular dysfunction and adverse remodeling: A sex-specific gene profiling analysis.心肌细胞特异性敲除 G 蛋白偶联雌激素受体(GPER)导致左心室功能障碍和不良重构:一种性别特异性基因谱分析。
Biochim Biophys Acta Mol Basis Dis. 2017 Aug;1863(8):1870-1882. doi: 10.1016/j.bbadis.2016.10.003. Epub 2016 Oct 8.
2
Overexpression of TREM2 enhances glioma cell proliferation and invasion: a therapeutic target in human glioma.TREM2的过表达增强胶质瘤细胞的增殖和侵袭:人类胶质瘤的一个治疗靶点。
Oncotarget. 2016 Jan 19;7(3):2354-66. doi: 10.18632/oncotarget.6221.
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Identification of high-copper-responsive target pathways in Atp7b knockout mouse liver by GSEA on microarray data sets.基于微阵列数据集的 GSEA 分析鉴定 Atp7b 敲除小鼠肝脏中的高铜反应靶途径。
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Microarray analysis reveals age-related differences in gene expression during the development of osteoarthritis in mice.微阵列分析揭示了小鼠骨关节炎发展过程中基因表达的年龄相关差异。
Arthritis Rheum. 2012 Mar;64(3):705-17. doi: 10.1002/art.33388.