Project description:We systematically assessed the transcriptomic changes of lipopolysaccharides (LPS) of mice upon stimulation with immunoglobulins (IVIg), modified immunoglobulins (modIVIg) or vehicle controls in kidney, blood and liver in vivo. Data indicate different in vivo responses to LPS in conjunction with IVIg, modIVIg or vehicle. RNA from murine liver and kidney tissues (LPS+vehicle, LPS+IVIg, LPS+modIVIg; four samples each group) as well as circulating leukocytes from WBC (three samples each group) was extracted and subject to microarray analysis for comparison of transcriptomic responses. Normalization and quality control was performed for each organ separately.
Project description:We systematically assessed the transcriptomic changes of lipopolysaccharides (LPS) of mice upon stimulation with immunoglobulins (IVIg), modified immunoglobulins (modIVIg) or vehicle controls in kidney, blood and liver in vivo. Data indicate different in vivo responses to LPS in conjunction with IVIg, modIVIg or vehicle.
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.
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.
Project description:Purpose: The goal of this study was to assess changes in the activated B cells transcriptome upon TENT5C knockout in mice Methods: RNA-Seq data were obtained for LPS-activated primary B cells isolated from either wild-type or TENT5C KO mice Results: Immunoglobulins transcripts were found to be downregulated in B cells isolated from TENT5C KO mice
Project description:This study describes the changes in epigenetic chromatin modifications during murine hematopoietic stem cell differentiation in vivo using a modified miniChIP-chip technology. We have addressed issues including bivalent (H3K4me3/H3K27me3) modifications, lineage priming hypothesis, and stem cell chromatin properties in our study described in Weishaupt et al., 2009 (Blood)
