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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression in human endothelial cell with innate immunity stimulation

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Hisanori Nishio

PROVIDER: E-GEOD-20929 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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