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Gene expression in fetal aortic arteries of C57BL/6 mice with Nod1 stimulation

ABSTRACT: We previously demonstrated that an innate immune receptor, the nucleotide-binding oligomerization domain-1 (Nod1), was involved in the vascular disease in young and adult mice. However, little is known about the role of Nod1 signaling in fetuses. We administered FK565, one of the Nod1 ligands, to pregnant C57BL/6 mice and examined its effect in the fetuses. Nod1 stimulation increased levels of cytokines in the pregnant mice, placentae and fetuses. We found that FK565 which was administered to the pregnant mice transferred to the fetuses through the placentae, and exerted its effects on fetuses in vivo. Nod1 was abundantly expressed in the arteries, and the vascular tissues predominantly produced CCL2 and IL-6 in response to FK565 compared with other fetal tissues. FK565 induced up-regulation of genes associated with immune response, inflammation and apoptosis in fetal vascular tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE65188 | GEO | 2016/01/31

SECONDARY ACCESSION(S): PRJNA273368

REPOSITORIES: GEO

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Gene expression in tissues of Mus musculus with innate immunity stimulation

Project description:This is an investigation of whole genome gene expression level in tissues of mice stimulated by LPS, FK565 or LPS + FK565 in vivo and ex vivo. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in aortic root including aortic valves, slight in aorta and absent in other arteries. The degree of respective vascular inflammation is associated with persistent high expression of proinflammatory chemokine/cytokine genes in each tissue in vivo by microarray analysis, and not with Nod1 expression levels. The ex vivo production of proinflammatory chemokine/cytokine by Nod1 ligand is higher in aortic root than in other arteries from normal murine vascular tissues, and also higher in human coronary artery endothelial cells (HCAEC) than in human pulmonary artery endothelial cells (HPAEC), suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular tissue/cell itself. A fourty chip study using total RNA recovered from four isolated tissues of mice which were stimulated by various reagents. Aortic root, pulmonary artery, aorta and spleen of mice in 3 groups: 1) intraperitoneal injection of 20M-NM-<g of LPS priming only, 2) oral administration of FK565 (100M-NM-<g) for consecutive days, 3) oral administration of FK565 (100M-NM-<g) for consecutive days 1 day after LPS priming, at day 2, 4, and 7. And six chip study using total RNA recovered from three isolated vascular tissues of mice which were stimulated by FK565 (10M-NM-<g/mL) ex vivo.

2011-03-01 | E-GEOD-20930 | biostudies-arrayexpress

Gene expression in tissues of Mus musculus with innate immunity stimulation

2011-03-01 | GSE20930 | GEO

Gene expression in human endothelial cell with innate immunity stimulation

2011-03-01 | GSE20929 | GEO

Gene expression in human endothelial cell with innate immunity stimulation

Project description:This is an investigation of whole genome gene expression level in human coronary endothelial cells (HCAEC) and human pulmonary endothelial cells (HPAEC) stimulated by FK565 or LipidA. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in and aortic root including aortic valves, slight in aorta and absent in other arteries. The in vitro production of proinflammatory chemokine/cytokine by FK565 is higher in HCAEC than in HPAEC, suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular cell itself. A six chip study using total RNA recovered from HCAEC and HPAEC which were stimulated by LipidA or FK565 in vitro. HCAEC and HPAEC were stimulated with FK565 (10µg/mL) or LipidA (100ng/mL) for 24 hours in 12-well plates (10,000 cells/cm2). Total RNA was extracted and subjected to RNA microarray analysis.

2011-03-01 | E-GEOD-20929 | biostudies-arrayexpress

Maternal Influenza A Virus Infection Restricts Fetal and Placental Growth and Adversely Affects the Fetal Thymic Transcriptome

Project description:Maternal influenza A viral infections in humans are associated with low birth weight, increased risk of pre-term birth, stillbirth and congenital defects. To examine the effect of maternal influenza virus infection on placental and fetal growth, pregnant C57BL/6 mice were inoculated intranasally with influenza A virus A/CA/07/2009 pandemic H1N1 or PBS at E3.5, E7.5 or E12.5, and the placentae and fetuses collecgted and weighed at E18.5. Fetal thymuses were pooled from each litter. Placentae were examined histologically, stained by IHC for CD34 and vascular channels quantified. RNA from E7.5 and E12.5 placentae and E7.5 fetal thymuses was subjected to RNA sequencing and pathway analysis. Placental weights were decreased in litters inoculated with influenza at E3.5 and E7.5. Placentae from E7.5 and E12.5 inoculated litters exhibited decreased labyrinth development and transmembrane protein 150A gene was upregulated in E7.5 placentae. Fetal weights were decreased in litters inoculated at E7.5 and E12.5 compared to controls. RNA sequencing of E7.5 thymuses indicated that 957 genes were downregulated 2-fold including Mal, which is associated with Toll-like receptor signaling and T cell differentiation. There were 28 upregulated genes. It is concluded that maternal influenza A virus infection impairs fetal thymic gene expression as well as restricting placental and fetal growth.

2020-09-11 | GSE157132 | GEO

Expression data from cardiac CD11c+MHC II+ cells

Project description:We previously reported that a synthetic Nod1 ligand, FK565, induced coronary arteritis in mice similar to Kawasaki disease. However, the molecular mechanisms underlying this site-specific inflammation have remained elusive. In this study, we found that CD11c+MHC class II+ cells accumulated in the heart of FK565-treated mice prior to arteritis development. We used microarray analysis to detail gene expression of CD11c+MHC class II+ cells. To obtain gene expression profile of CD11c+MHC class II+ cells, we isolated these cells from hearts of FK565-treated mice. Briefly, female mice at 8weeks age were administered 500 μg of FK565 subcutaneously at day 0 and day 3. At day6, murine hearts were removed and digested with collagenase. CD11c+MHC II+ cells were sorted as PI–CD45+Ly6G–NK1.1–CD11b+CD11c+MHC II+ using FACS Aria cell sorter (BD Biosciences). Sorted cells were subjected to RNA preparation. Two independent replicates from ten mice were made.

2015-03-31 | E-GEOD-60506 | biostudies-arrayexpress

Expression data from cardiac CD11c+MHC II+ cells

2015-03-31 | GSE60506 | GEO

Gene expression in aortic roots of Apoe KO mice with Nod1 stimulation

Project description:To explore the mechanisms underlying progression of atherosclerosis provoked by Nod1 ligand stimulation, we performed microarray gene expression profiling of aortic roots of 6- and 9-week-old Apoe KO mice with or without oral FK565 administration. A gene ontology analysis of the genes up-regulated in FK565-administrated group at both time points showed that a number of biological process terms were associated with immune response. Among chemokine/cytokine genes, we observed that only 3 genes such as Ccl5, Ccl8 and Cxcl16 elevated more than 2-fold in response to oral administration of FK565 at both time points. An eight chip study using total RNA recovered from aortic roots in Apoe KO mice with or without FK565 administration, at the age of 6 and 9 weeks. Two independent experiments were performed in each group. In FK565-administrated groups, mice were orally administrated FK565 (50 µg) twice a week for 1 or 4 weeks from 5 weeks of age.

2014-11-06 | E-GEOD-48947 | biostudies-arrayexpress

Gene expression in aortic roots of Apoe KO mice with Nod1 stimulation

2014-11-06 | GSE48947 | GEO

Genome-wide analysis of the transcriptional response to porcine reproductive and respiratory syndrome virus infection at the maternal/fetal interface and in the fetus

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