Project description:Comparing control and LPS-administered with either 40 mg/kg LPS for early time points (ETP) or 10 mg/kg for late time points (LTP). In ETP, 7-7 animals were sacrificed at 1.5 and at 6 hours after LPS administration. In LTP, 7-7 animals were sacrificed at 24 and 48 hours after the endotoxin injection. In both ETP and LTP 7 mice were received equal volume of saline to use as negative control. Four animals were selected for miRNA microArray analysis based on their proinflammatory (TNF-α and IL-6) mRNA expression levels.
Project description:Mice intraperitoneally administered with LPS and Stx exhibit HUS-like pathology. While mouse and human Gb3 localization is different, LPS and Stx induced kidney injury models in mice have been used to confirm responsiveness to various stx-related inflammatory pathways and treatments. In order for this mouse model to apply tHUS in humans, more detailed and exhaustive comprehension of this animal model is needed. Although molecular studies have been conducted on this mouse model before, we consider that there is still scope for further investigation of molecular pathways and studies on kidney damage segments. Overall, Biological pathways, upstream regulators, and downstream biological activities occurring in the kidney after LPS/Stx administration were identified through Ingenuity Pathway Analysis ™ using the result of microarray. In addition, we identified the detailed damaged site in the renal tubule from the down-regulation gene revealed by microarray.
Project description:Cows were fed a lactation diet at ad libitum intake (n = 6). At 27±3 days in milk, cows were injected with 50 µg of LPS E. coli in one healthy rear mammary quarter. Milk samples were collected just before LPS challenge (LPS-) and 6.5 h after LPS challenge (LPS+) from the same cows. Microarray analysis was performed using customized 8x60K ruminant miRNA microarrays to compare LPS- to LPS+ miRNome. MiRNome comparison between LPS- and LPS+ identified 37 differentially abundant miRNAs (q-value ≤ 0.05)
Project description:Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation.
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:Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation. Mice were given intracerebroventricular injections of saline vehicle (n = 4) or lipopolysaccharide (n = 4). Twenty-four hours later, we dissected the hippocampus and cerebral cortex and processed the tissue for microarray analysis. Gene expression changes observed in the microaray data were validated with quantitative real-time PCR.
Project description:The aim of this study was to identify miRNAs that regulate AKI and develop their applications as diagnostic biomarkers and therapeutic agents. First, kidney tissues from two different AKI mouse models, namely, AKI induced by the administration of lipopolysaccharide (LPS) causing sepsis (LPS-AKI mice) and AKI induced by renal ischemia–reperfusion injury (IRI-AKI mice), were exhaustively screened for their changes of miRNA expression compared with that of control mice by microarray analysis.