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

Data Brief

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; Cardiovascular Research Center, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA; Sticht Center on Aging, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA.

Published: February 2017

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5198850PMC
http://dx.doi.org/10.1016/j.dib.2016.11.057DOI Listing

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