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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE100635 | GEO | 2019/12/26

REPOSITORIES: GEO

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Project description:In order to study the gene expression profile in C57Bl/10 mouse blood, we exposed three different groups of animals. First was exposed to PO2 21% or normoxia. The second was exposed to chronic hypoxia (from PO2 21% to PO2 8%) and the third was also exposed to the same chronic hypoxia (CH) protocol but followed by two weeks under normoxia, and called as recovery group. The blood was extracted from inferior vena cava, the RNA was extracted, amplified and hybridized to Affimetrix MOE 430 V2.o chip. The results were analyzed using Partek Genome suite software. Using two fold cuttoff and 0% FDR parameters, we observed genes 512 diferentially expressed, of which one gene was up-regulated in both hypoxic and recovery condition, 202 were up-regulated during CH and then down-regulated after the recovery, 18 genes were down-regulated afteh CH and the up-regulated after recovery, ans finally 9 genes were down-regulated in both CH and recovery conditions. Each group of C57Bl/10 mouse had 4 individuals and they were divided into three different groups of animals. First was exposed to PO2 21% or normoxia for 14 days. The second was exposed to chronic hypoxia (from PO2 21% to PO2 8%) and the third was also exposed to the same chronic hypoxia (CH) protocol but followed by two weeks under normoxia, and called as recovery group. After the exposure period, the animals were anaesthetized with a mix of Ketamine (100 mg/mL) and xylasine (20 mg/mL) in a proportion of 1:1. A incison was made on abdominal area and from kidneis and liver area of inferior vena cava venus blood was collected The blood was extracted from inferior vena cava. Then, the RNA was extracted, amplified and hybridized to Affimetrix MOE 430 V2.o chip. The results were analyzed using Partek Genome suite software. Using two fold cuttoff and 0% FDR parameters, we observed genes 512 diferentially expressed, of which one gene was up-regulated in both hypoxic and recovery condition, 202 were up-regulated during CH and then down-regulated after the recovery, 18 genes were down-regulated afteh CH and the up-regulated after recovery, ans finally 9 genes were down-regulated in both CH and recovery conditions.

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

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