PLX253441

GSE100635: Histamine H3 receptor agonist regulates the expression of inflammation-related genes in kidney and heart of ANS-treated mice

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

We found the impaired renal function accompanied with severe cardiac dysfunction in mice co-treated with angiotensin II, nephrectomy and salt (ANS), and identified the increased level of plasma histamine in ANS-treated mice. Interestingly, pro-inflammatory genes were increased in kidneys of ANS-treated animals, which were down-regulated by histamine H3 receptor (H3R) agonist. Purpose: To evaluate the molecular mechanisms underlying the effect of the H3R agonist on the ANS-induced renal and cardiac inflammation, we performed a comprehensive analysis of ANS-mediated gene expression changes with/without H3R agonist in kidneys and hearts using RNA sequencing (RNA-Seq). Results: To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) among three groups, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software. In comparison with the control of kidney group, 1,283 (1,010 up- and 273 down-regulated) unique genes were significantly changed in the ANS-treated group. Meanwhile, the data set of ANS-treated kidneys with H3R agonist revealed significant changes in 234 (65 up- and 169 down-regulated) genes as compared with the control groups. In case of hearts, the ANS-treated group revealed that 85 (66 up- and 19 down-regulated) unique genes were significantly changed compared to the control groups. Furthermore, in comparison with the ANS-treated with H3R agonist group, one up-regulated gene was significantly changed in the ANS-treated group. SOURCE: Jun-Dal KimFukamizu Lab. University of Tsukuba