Genome-wide identification and analysis of gene expression in BV-2, a murine microglial cell line, infected with rabies virus CVS-11 (Challenge virus standard)
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Pingsen Zhao
PROVIDER: E-GEOD-35684 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Host-virus interaction was analyzed at gene expression level. The hypothesis tested in the present study was that rabies virus (RABV) infection affects the gene expression in brains of mice and RAB with different virulence induce distinct expression pattern in host. Results provide important information that RABV infection led to alteration of gene expression in brains of mice and FJDRV, a street rabies virus with highly virulence isolated from brain of rabid dog in Fujian provice of China, or ERA, a laboratory-adapted rabies virus with lower virulence induced different expression pattern, including immune-related and cellular signaling-related genes. An eighteen chip study was performed using total RNA isolated from brains in Treatment 1, three BALB/c mice infected with FJDRV, Treatment 2, three BALB/c mice infected with ERA, and Control, three BALB/c mice non-infected and all treatments were performed with two technical replicates.
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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Project description:This SuperSeries is composed of the following subset Series: GSE26269: Genome-wide identification and analysis of microRNA expression in brains of mice infected with FJDRV, a street rabies virus with high virulence, and ERA, a laboratory-adapted virus with lower virulence GSE26270: Genome-wide identification and analysis of gene expression in brains of mice infected with FJDRV, a street rabies virus with high virulence, and ERA, a laboratory-adapted virus with lower virulence Refer to individual Series
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Project description:Genipin is a natural blue colorant in food industry. Inflammation is correlated with human disorders, and nuclear factor-κB (NF-κB) is the critical molecule involved in inflammation. In this study, the anti-inflammatory effect of genipin on the lipopolysaccharide (LPS)-induced acute systemic inflammation in mice was evaluated by NF-κB bioluminescence-guided transcriptomic analysis. Transgenic mice carrying the NF-κB-driven luciferase genes were administered intraperitoneally with LPS and various amounts of genipin. Bioluminescent imaging showed that genipin significantly suppressed LPS-induced NF-κB-dependent luminescence in vivo. The suppression of LPS-induced acute inflammation by genipin was further evidenced by the reductions of cytokine levels in sera and organs. Microarray analysis of these organs showed that the transcripts of 79 genes were differentially expressed in both LPS and LPS/genipin groups, and one third of these genes belonged to chemokine ligand, chemokine receptor, and interferon (IFN)-induced protein genes. Moreover, network analysis showed that NF-κB played a critical role in the regulation of genipin-affected gene expression. In conclusion, we newly identified that genipin exhibited anti-inflammatory effects in a model of LPSinduced acute systemic inflammation via downregulation of chemokine ligand, chemokine receptor, and IFN-induced protein productions. A total of 25 transgenic mice (female, 6 to 8 weeks old) were randomly divided into five groups of five mice: (1) mock, no treatment; (2) LPS (4 mg/kg), (3) LPS plus genipin (1 mg/kg), (4) LPS plus genipin (10 mg/kg), and (5) LPS plus genipin (100 mg/kg). Mice were challenged intraperitoneally with LPS and then with genipin 10 min later. Four hours later, mice were imaged for the luciferase activity, and subsequently sacrificed for ex vivo imaging, RNA extraction, and immunohistochemical staining.
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Project description:The aim of this study was to analyze the host responses to ionizing radiation by nuclear factor-κB (NF-κB) bioluminescence imaging-guided transcriptomic tool. Transgenic mice, carrying the NF-κB-driven luciferase gene, were exposed to a single dose of 8.5 Gy total-body irradiation. In vivo imaging showed that a maximal NF-κB-dependent bioluminescent intensity was observed at 3 h after irradiation and ex vivo imaging showed that liver, intestine, and brain displayed strong NF-κB activations. Microarray analysis of these organs showed that irradiation altered gene expression signatures in an organ-specific manner. Pathway analysis showed that pathways associated with metabolism and immune system were altered primarily in liver and intestine. the upregulation of fatty acid binding protein 4, serum amyloid A2, and serum amyloid A3, which are participated in both inflammation and lipid metabolism, suggesting that irradiation might affect the cross pathways of metabolism and inflammation. Moreover, The upregulation of chemokine (CC-motif) ligand 5, chemokine (CC-motif) ligand 20, and Jagged 1 genes suggested that these genes might contribute to the radiation enteropathy. Male transgenic mice (6 to 8 weeks old) were exposed to a single dose of whole-body X-rays generated at 6 MV (Clinac® 21EX medical linear accelerator, Varian, Palo Alto, CA, USA) and at a dose rate of 4 Gy/min. Mice were imaged at 0 h, 1 h, 3 h, 9 h, 24 h, 48 h, or 72 h, or on 7 d or 14 d after irradiation with 8.5 Gy. RNAs were extracted at 3 h after irradiation.
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Project description:Chitosan has been widely used in food industry as a weight-loss aid and a cholesterol-lowering agent. Previous studies have shown that chitosan affects metabolic responses and contributes to anti-diabetic, hypocholestermic, and blood glucose-lowering effects; however, the in vivo targeting sites and mechanisms of chitosan remain to be clarified. In this study, we constructed transgenic mice which carried the luciferase genes driven by peroxisome proliferator-activated receptor (PPAR), a key regulator of fatty acid and glucose metabolism. Bioluminescent imaging of PPAR transgenic mice was applied to report the organs that chitosan acted on, and gene expression profiles of chitosan-targeted organs were further analyzed to elucidate the mechanisms of chitosan. Bioluminescent imaging showed that constitutive PPAR activities were detected in brain and gastrointestinal tract. Administration of chitosan significantly activated the PPAR activities in brain and stomach. Microarray analysis of brain and stomach showed that several pathways involved in lipid and glucose metabolism were regulated by chitosan. Moreover, the expression levels of metabolism-associated genes like apolipoprotein B (apoB) and ghrelin genes were down-regulated by chitosan. In conclusion, these findings suggested the feasibility of PPAR bioluminescent imaging-guided transcriptomic analysis on the evaluation of chitosan-affected metabolic responses in vivo. Moreover, we newly identified that downregulated expression of apoB and ghrelin genes were novel mechanisms for chitosan-affected metabolic responses in vivo . Mice (6 to 8 weeks old) were subcutaneously injected saline or 0.2 g/kg chitosan. Chitosan oligosaccharide lactate (MW=4000-6000, >90% deacetylation) was purchased from Sigma-Aldrich (St. Louis, MO, USA) and dissolved in DDW. For rosiglitazone treatment, mice were orally administered 50 mg/kg rosiglitazone. Mice were then imaged for the luciferase activity or sacrificed for microarray analysis at indicated periods.
2014-10-29 | E-GEOD-33565 | biostudies-arrayexpress
Project description:In this study, a novel IR-binding protein (IRBP) from Momordica charantia, named as mcIRBP, was identified by analyzing the physical and functional interactions between mcIRBP and IR. The hypoglycemic effect and mechanism of mcIRBP were further evaluated in normal and streptozotocin-induced diabetic mice. Normal and diabetic mice were treated without or with mcIRBP and RNAs from muscle tissues were extracted for microarray analysis. Number of replicate was three.
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