Project description:Background: Transcriptome analysis has been used in autism spectrum disorder (ASD) to unravel common pathogenic pathways based on the assumption that distinct rare genetic variants or epigenetic modifications affect common biological pathways dysregulated in ASD. To unravel recurrent ASD-related neuropathological mechanisms, we took advantage of the En2-/- mouse model and performed transcriptome profiling on cerebellar and hippocampal adult tissues. Methods: En2-/- and WT cerebellar and hippocampal tissue from littermate mice were assessed for differential gene expression using microarray hybridization followed by RankProd analysis. To identify functional categories overrepresented in the differentially expressed genes we used the BIOBASE ExPlain system and mouse phenotype ontology database. Furthermore, we performed direct enrichment analysis of ASD associated genes from the SFARI repository in our differentially expressed genes. Results: We found 842 differentially expressed genes in En2-/- cerebellum and 862 in the En2-/- hippocampus. Our functional analysis revealed that the molecular signature of En2-/- cerebellum and hippocampus shares convergent pathological pathways with ASD, including abnormal synaptic transmission, altered developmental processes and increased immune response. Furthermore, when directly compared to the repository of the SFARI database, our differentially expressed genes show enrichment of ASD-associated genes significantly higher than previously reported. Among the differentially expressed genes 20 were validated by quantitative PCR. Conclusions: Our results indicate the En2-/- mouse model of ASD as an appropriate tool to investigate molecular alterations related to ASD. En2-/- and WT cerebellar and hippocampal tissue from 3 littermates mice for each genotype was hybridized on three replicates microarrays.
Project description:Wild-type mice or mice lacking the expression of CHIP (Stub1) were subjected to either sham surgery (Sham) or trans-aortic banding (TAB). After one week, RNA was extracted from heart and run on the Agilent 4x44K gene expression array to look at differences in the cardiac transcriptional response to pressure overload-induced hypertrophy in the absence of CHIP. Four-condition experiment: WT vs. CHIP(-/-) with SHAM or TAB surgery. Biological replicates: 4 per condition.
Project description:Silkworms show a reproductive behavior induced by sex pheromone. To elucidate the neral mechanism of sex pheromone induced sexual behavior in the silkworm, we attempted to use the neural activity-induced gene as a neural activity marker. Since no neural activity-induced gene was identified in the silkworm, we conducted screening of neural activity-induced gene using the male silkworm brain. By the screening, we identified Bhr38 as a novel neural activity-induced gene, and succeded to comprehensively map the active neruons in the silkworm brain in response to the sex pheromone exposure. Further, we found that Dhr38, the Drosophila homologue of Bhr38, also expressed in a neural activity dependent manner. These results strongly suggest that Hr38 is a highly conserved neural activity-induced gene. The male silkworms were exposed to the female odor for 30 min (group P). Non-treated male silkworms were used as the control group group C. Ten brains were collected for each sample and stored at -80°C until use. Total RNA was isolated by the TRIzol reagent and subjected to microarray experiments using the custam made (8x16k) Oligo Microarray (Agilent Technologies, Inc.).
Project description:Analysis of glomeruli isolated from kidneys of 4 month male BXSB/MpJ-Yaa. The BXSB/MpJ-Yaa mouse strain is a lupus-prone model. Results provide insight into the pathogenic mechanisms linked to glomerulonephritis in BXSB/MpJ-Yaa mice. The glomeruli were isolated from 6 BXSB/MpJ-Yaa (glomerulonephritis model) and BXSB/MpJ-Yaa+ (control). 6 glomerular populations of each strain were devided into 3 groups (1 group / 2 populations). 3 glomerulonephritis models versus 3 controls analysis was performed. BXSB/MpJ-Yaa is a recombinant inbred strain developed originally from a C57BL/6 female mouse and a SB/Le male mouse. Yaa (Y-linked autoimmune accelerator locus) localizing on the Y chromosome of BXSB/MpJ-Yaa male mice is the result of a duplication of an about 4 Mbp telomeric segment near the pseudoautosomal region of the X chromosome onto the Y chromosome. BXSB/MpJ-Yaa+ (control) male mice carry the wild-type Y chromosome in place of the mutant Yaa-containing Y chromosome of BXSB/MpJ-Yaa male mice.
Project description:We compared gene expression profiles between testes from C57BL/6 and C57BL/6-background congenic mouse strain B6.MRLc1-(D1Mit202M-bM-^@M-^SD1Mit403) carrying the telomeric region of MRL-type Chr 1 (67.97M-bM-^@M-^S81.63 cM) at 10 days after a single scrotal heat stress of 43M-BM-0C for 20 min. Heat-induced gene expression in mouse testis was measured at 10 days after a single heat exposure. The testes were isolated from 3 C57BL/6 and 3 B6.MRLc1-(D1Mit202M-bM-^@M-^SD1Mit403). C57BL/6 versus B6.MRLc1-(D1Mit202M-bM-^@M-^SD1Mit403) analysis was performed.
Project description:To further development of gene expression in inflammatory bowel disease(IBD), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish IBD patients and healthy volunteers. Colon biopsies were obtained from IBD patients and healthy volunteers during endoscopy. There were 353 genes that showed greater than 4-fold differential expression (285 upregulated and 68 downregulated) between IBD patients and healthy volunteers. Colon biopsies were obtained from 3 CD and age- ,sex- mathed healthy controlspatients and 3 healthy volunteers during endoscopy.
Project description:To understand allopoyploid speciation into hydrologically fluctuating niches, we observed gene expressions of two parental species and their allotetraploid species under wet and dry conditions Gene expression of leafs from control, dry and wet conditions over three Caramine species: C. amara, C. hirsuta and C. flexuosa
Project description:Mastitis is an inflammation of the mammary gland (MG), usually due to bacterial infection. Although considerable attention has been paid to this economically important disease, the early stages of the host response remain poorly defined. In particular, it is unclear how mammary epithelial cells (MEC), a first barrier against pathogens, respond to infection. Indeed, it is difficult to differentiate between the contributions of MEC and infiltrating immune cells to gene expression profiles of mammary tissue during mastitis. The current investigation examines the response of MEC at the early stage of infection using a non invasive RNA sampling method taking advantage of the presence of cytoplasmic crescents contained in milk fat globules. We have recently shown that, in goats, Milk Fat Globules (MFG) provide a unique source of RNA to study the in vivo regulation of gene expression in MEC. This non invasive RNA sampling method was used during the time course of an experimental intra mammary infection (IMI) with S. aureus. Experiments were performed using ovine microarrays (Agilent) to compare gene expression patterns before infection, at 12h, 18h and 24h post-infection (PI). Furthermore, we combined this approach with laser capture microdissection of MEC isolated from frozen slides of mammary tissue to study some specific genes at the late stage of infection (30h PI). We show that at 18h PI, before the burst of somatic cells in milk, MEC play an important role in the recruitment and activation of inflammatory cells through the IL-8 signaling pathways. Then, at the late stage of infection (30h PI), the contribution of MEC in immune response changes to produce different acute phase proteins, including SAA3, serpin A1 and PTX3. These cells also express factors that contribute directly to fighting infection, such as S100A12. In summary, we demonstrate for the first time in vivo how MEC orchestrate innate immune response during an IMI with S. aureus in the goat species. We report here new opportunities to assess the dynamics of gene expression in the mammary gland, thus providing significant advances in the understanding of MEC immune capacity.M-bM-^@M-^BFurthermore, the production of some molecules by MEC, in the early stages of IMI, could provide sensitive biomarkers for early detection and therefore, treatment of mastitis. Experiments were performed using ovine microarrays (Agilent) to compare gene expression patterns before infection, at 12h, 18h and 24h post-infection (PI). 20 sample records; mono-colour experimental design
Project description:By identifying differentially expressed LncRNAs/mRNAs in THP-1 macrophages and THP-1 macrophage-derived foam cells, we select some differentially expressed LncRNAs and explore their roles in atherosclerosis process. We already find that some LncRNA can effect cholesterol metabolism and level of inflammation factor, which may influence atherosclerosis process. In the study presented here, 6 human samples were used to acquire expression profiles, which provide futher insight into the pathologies of atherosclerosis
Project description:Sorafenib is associated with cardiac adverse effects, including left ventricular dysfunction. However, the precise mechanism remains unclear. Here, we aimed to establish the genes responsible for this cardiotoxicity using zebrafish. A pigmentless zebrafish line expressing green fluorescent protein in the heart were treated with or without sorafenib. In vivo fluorescent cardiac imaging revealed that the ventricular dimension of the longitudinal axis in zebrafish treated with sorafenib was significantly lower than in those without sorafenib. Transcriptome analysis of zebrafish hearts revealed that expression of stanniocalcin1 (stc1) in zebrafish treated with sorafenib was significantly lower than that without sorafenib treatment. We were able to demonstrate that the ventricular dimension of the longitudinal axis in stc1 morphant was significantly smaller than that of control zebrafish and that forced expression of stc1 normalized the decrease in ventricular diameter in stc1 morphant and zebrafish treated with sorafenib. These data suggest that stc1 is the gene responsible for sorafenib-induced cardiotoxicity. Gene expression regulated by sorafenib in zebrafish at 4 dpf was measured. Four independent experiments were performed for each group.