Project description:MicroRNAs (miRNAs), a class of noncoding RNAs measuring 18 to 23 nucleotides (nt) that play important regulatory roles in host-virus interactions. Avian-origin H3N2 canine influenza virus (CIV) has emerged as the most prevalent subtype among dogs in Asia since 2007. To evaluate the roles of host miRNAs in H3N2 CIV infection, here, miRNA profiles obtained from primary canine bronchiolar epithelial cells (CBECs) and canine alveolar macrophages (CAMCs) were compared between infected and mock-infected cells with the H3N2 CIV JS/10. It was found that cfa-miR-125b, cfa-miR-151 and cfa-miR-423a expressions were significantly decreased in CIV-infected canine primary cells. Bioinformatics prediction indicated that 5’ seed regions of three miRNAs are partially complementary to the mRNAs of nucleoprotein (NP) and non-structural protein 1 (NS1) of JS/10. As determined by virus titration, quantitative real-time PCR (qRT-PCR) and western blotting, overexpression of cfa-miR-125b and cfa-miR-151 inhibited CIV infection, whereas overexpression or inhibition of cfa-miR-423a inhibited this infection. These results indicated that CIV replication could be regulated by miRNAs from host cells infected with CIV. Our findings support the notion that cellular miRNAs can inhibit virus infection, help to elucidate the resistance of host cells to viral infection and to clarify the pathogenesis of H3N2 CIV. We used microarrays to detail the global programme of gene expression of primary canine alveolar macrophages (CAMCs) compared between infected and mock-infected cells with the H3N2 canine influenza virus (CIV) JS/10.
Project description:Microarrays was performed in 7 aCGH-matched canine primary tumors (4 DLG2 deleted, 3 DLG2 wild type) to investigate the gene expression profiles associated with DLG2 deletion in canine osteosarcoma.
Project description:We used microarray to detect pathway differences in the hippocampus in mucopolysaccharidosis type VII ( MPS VII ), a mouse model of a lysosomal storage disease Pathway changes were similar to those found in different strain where MPS VII mutation was backcrossed on a C3h-heouj background and implicated immune, vesicle and other pathways
Project description:Human colorectal cancer (CRC) is one of the better-understood systems for studying the genetics of cancer initiation and progression. To develop a cross-species comparison strategy for identifying CRC causative gene or genomic alterations, we performed array comparative genomic hybridization (aCGH) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported for human CRCs, in 10 spontaneously occurring canine CRCs. The results revealed for the first time a strong degree of genetic homology between sporadic canine and human CRCs. First, we saw that between 5 and 22% of the canine genome was amplified/deleted in these tumors, and that, reminiscent of human CRCs, the total altered sequences directly correlated to the tumor’s progression stage, origin, and likely microsatellite instability status. Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted that the canine orthologs of genes participating in known human CRC pathways were recurrently disrupted, indicating that these pathways might be altered in the canine CRCs as well. Lastly, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from the two species were clustered according to the tumor subtypes but not the species. Significantly, compared with the shared CNAs, we found that species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that harbor more segmental duplications and interspecies genomic rearrangement breakpoints. These findings indicate that CNAs recurrent between human and dog CRCs may have a higher probability of being cancer-causative, compared with CNAs found in one species only
Project description:To investigate the canine mammary gland tumor, we established 8 cell lines We then performed gene expression profiling analysis using data obtained from RNA-seq of 10 different cells.
Project description:Human DUX4 and mouse Dux transcription factors are normally expressed in the germ line and early embryonic cells where they activate the cleavage stage genes. The misexpression of DUX4 in skeletal muscles causes Facioscapulohumeral dystrophy (FSHD). In primates and rodents, DUX4 and Dux arose from retrotransposition of the mRNA from the ancestral intron-containing DUXC, which is not found in these species, and whether it has similar roles in the cleavage stage and FSHD as DUX4 and Dux are unknown. Here, we identified two isoforms of DUXC in canine testis tissues: One encodes the canonical double homeodomain (DUXC) similar to DUX4/Dux, and one contains an extra exon that disrupts the conserved amino-acid sequence of the first homeodomain (DUXC-ALT). We expressed DUXC and DUXC-ALT in canine skeletal muscle and found that the expression of DUXC induced retrotransposons and pluripotent programs similar to DUX4 and Dux, whereas DUXC-ALT did not robustly activate genes in these assays.
Project description:We used RNAseq to investigate innate immune responsiveness in canine 030-D cell line induced by inactivated L. interrogans serogroups Canicola and Icterohaemorrhagiae, and two bivalent, non-adjuvanted canine Leptospira vaccines containing the same serogroups. We identified more than 900 DEGs associated with pathways related to innate immune responses in common to these three stimuli. Several molecules including CXCL-10, SAA, and complement factor C3 were identified that could serve as targets for development of a biomarker-based in vitro assay to assess Leptospira vaccine quality. In vitro assay could replace the current animal vaccine-challenge potency assay and contribute to reduction of animal use in vaccine manufacturing.
Project description:We used microarray to detect pathway differences in the various brain regions in a monogenic in mucopolysaccharidosis type VII ( MPS VII ), a mouse model of a lysosomal storage disease A number of changes revealed unexpected system and process alterations, such as upregulation of the immune system with few inflammatory changes (a significant difference from the closely related MPS IIIb model), down-regulation of major oligodendrocyte genes even though white matter changes are not a feature histopathologically, and a plethora of developmental gene changes.