Data in Brief 10 (2017) 465–473
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Data in Brief
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Data Article Inflammatory and mitochondrial gene expression data in GPER-deficient cardiomyocytes from male and female mice
Hao Wang a,b, Xuming Sun a, Jeff Chou c, Marina Lin a, Carlos M. Ferrario d,e, Gisele Zapata-Sudo a,f, Leanne Groban a,b,g,h a Department of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA b Internal Medicine/Molecular Medicine, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA c Public Health Sciences, Section on Biostatistical Sciences, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA d Department of Surgery, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA e Department of Internal Medicine/Nephrology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA f Institute of Biomedical Sciences, Drug Development Program, Federal University of Rio de Janeiro, Brazil g Cardiovascular Research Center, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA h Sticht Center on Aging, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA
DOI of original article: http://dx.doi.org/10.1016/j.bbadis.2016.10.003 E-mail addresses: [email protected] (H. Wang), [email protected] (L. Groban). http://dx.doi.org/10.1016/j.dib.2016.11.057 2352-3409/& 2016 The Authors. Published by Elsevier Inc. All rights reserved. 466 H. Wang et al. / Data in Brief 10 (2017) 465–473
article info abstract
Article history: We previously showed that cardiomyocyte-specific G protein- Received 6 October 2016 coupled estrogen receptor (GPER) gene deletion leads to sex- Accepted 15 November 2016 specific adverse effects on cardiac structure and function; altera- Available online 23 November 2016 tions which may be due to distinct differences in mitochondrial Keywords: and inflammatory processes between sexes. Here, we provide the Cardiomyocyte results of Gene Set Enrichment Analysis (GSEA) based on the DNA GPER microarray data from GPER-knockout versus GPER-intact (intact) Knockout cardiomyocytes. This article contains complete data on the mito- Microarray chondrial and inflammatory response-related gene expression Mitochondria changes that were significant in GPER knockout versus intact Inflammation 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 remo- deling: 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. & 2016 The Authors. Published by Elsevier Inc. All rights reserved.
Specifications Table
Subject area Biology More specific sub- Heart disease, gene knockdown ject area Type of data Tables How data was Microarray data in cardiomyocytes generated using Affymetrix GeneAtlas 30-IVT acquired Express Kit Data format Analyzed Experimental Comparison of inflammatory and mitochondrial gene expression profiles of factors GPER-deficient versus intact cardiomyocytes from male and female mice Experimental RNA isolation, global gene expression analysis, and bioinformatics analyses features using Gene Set Enrichment Analysis (GSEA) software Data source Wake Forest School of Medicine, Winston-Salem, NC, USA location Data accessibility Dataset is within this article and available in the Gene Expression Omnibus with accession number GEO: GSE86843.
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