Transcriptome data analyses of prostatic hyperplasia in Esr2 knockout rats

• Published in: Data in brief 2019-06, Vol.24, p.103826-103826, Article 103826
• Main Authors: Khristi, Vincentaben, Ghosh, Subhra, Chakravarthi, V. Praveen, Wolfe, Michael W., Rumi, M.A. Karim
• Format: Article
• Language: English
• Subjects: Biochemistry, Genetics and Molecular Biology
• ISSN: 2352-3409; 2352-3409
• DOI: 10.1016/j.dib.2019.103826

Estrogen signaling plays an important role in the pathophysiology of prostatic hyperplasia. While signaling through estrogen receptor alpha (ESR1) increases proliferation of stromal cells, estrogen receptor beta (ESR2) plays an anti-proliferative and differentiating role in glandular epithelium. Disruption of ESR2 signaling resulted in prostatic glandular hyperplasia in the rat. To identify the ESR2-target genes, and the molecular mechanisms involved, we performed RNA-seq analyses in prostate glands of Esr2 knockout (Esr2−/−) and age matched wildtype rats. The raw data were analyzed using CLC genomics workbench. High quality RNA-seq reads were aligned to the Rattus norvegicus genome. Differentially expressed genes were identified based on an absolute fold change of 2 with pValue ≤0.05. Of the total 32,623 genes detected, 824 were differentially expressed in Esr2−/− prostate glands, 550 downregulated and 274 upregulated. Pathway analyses identified altered expression of genes involved in epithelial proliferation and benign tumor formation.