Project description:Primary outcome(s): Relationship with mRNA expression of B7 family molecules in blood of patients with colorectal cancer and clinicopathological factors
Project description:HCMV glycoproteins US7 and US8 target the innate immune response. We used microarrays to detail the global programme of gene expression and identified to down-regulated genes by US7 or US8.
Project description:The change of mRNA expression in murine immortalized podocyte were analyzed after miR-26a silencing. These results provide a basical information of molecular pathology in podocyte biology.
Project description:Nonsteroidal anti-inflammatory drugs (NSAIDs) has been suggested as adjunctive anti-tumor agents in human and veterinary medicine. However, its anti-tumor molecular machinery is still controversial. Therefore, we performed whole transcriptome analysis to discover gene expression influenced by NSAIDs treatment. A canine melanoma cell line (Mi/CMM1) was treated by three NSAIDs, piroxicam, carprofen, and robenacoxib, at their half maximal (50%) inhibitory concentrations (116 µM, 779 µM, and 156 µM) for 6 hours. Subsequently, total RNA were extracted and microarray analysis was performed to evaluate change in gene expression caused by NSAIDs treatment. Each condition had three biological replicates.
Project description:Mutations in pre-mRNA processing factors (PRPFs) cause autosomal dominant retinitis pigmentosa (RP), but it is unclear why mutations in ubiquitously expressed genes cause retinal disease. We have generated transcriptome profiles from RP11 (PRPF31-mutated) patient-derived retinal organoids and retinal pigment epithelium (RPE), as well as Prpf31+/- mouse tissues, which revealed that disrupted alternative splicing occurred for specific splicing programmes. Mis-splicing of genes encoding pre-mRNA splicing proteins was limited to patient-specific retinal cells and Prpf31+/- mouse retinae and RPE. Mis-splicing of genes implicated in ciliogenesis and cellular adhesion was associated with severe RPE defects that include disrupted apical-basal polarity, reduced trans-epithelial resistance and phagocytic capacity, and decreased cilia length and incidence. Disrupted cilia morphology also occurred in patient-derived photoreceptors, associated with progressive degeneration and cellular stress. In situ gene-editing of a pathogenic mutation rescued protein expression and key cellular phenotypes in RPE and photoreceptors, providing proof-of-concept for future therapeutic strategies.