Project description:To identify putative miRNA targets for uc.372, we overexpressed uc.372 in HepG2 cells and carried out a microarray analysis. A total of 66 miRNAs present in the array demonstrated 1.5-fold upregulation or downregulation of expression upon uc.372 transfection.
Project description:Primary objectives: Study the chemopreventive potential of 5-aminosalicylic acid (5-ASA) and ursodeoxycholic acid (UDCA) in UC by evaluating the effect of treatment on abberant crypt foci (ACF) number, size and rate of dysplasia.
Primary endpoints: 1) Study the chemopreventive potential of 5-ASA and UDCA in UC by evaluating the effect of treatment on ACF number.2) Gain mechanistic insight into the chemopreventive properties of 5-ASA and UDCA by genome-wide array based mRNA expression analysis of UC normal colonic mucosa before and after treatment.
Project description:Ulcerative colitis (UC) is a chronic inflammatory disease of the colon with preiods of active disease followed by remission. We performed a whole-genome transcriptional analysis of colonic biopsies from patients with histologically active and inactive UC, as well as non-inflammatory controls. Ulcerative colitis patients and non-inflammatory controls were collected for RNA extraction and hybridization on Affymetrix microarrays. Inclusion criteria for UC patients were: age between 18 and 65, diagnosis of UC established at least 6 months before inclusion and exclusion of concomitant infection. Active disease was defined by endoscopic and histologic score: Mayo sub score >=2 and MATTS >=3 respectively . Inactive disease was also defined by endoscopic and histologic score: Mayo sub score =0 and MATTS <=2 respectively, and a remission state for a minimum of 5 month prior to biopsy collection, and remained inactive for at least 6 months after. Uninvolved mucosa from patients with active UC was defined as a colonic segment with completely normal endoscopic appearance, normal histology, and absence of any previous evidence of active disease. Finally, a total of 43 biopsies were analyzed: 13 healthy controls, 8 inactive UC, 7 non-involved active UC and 15 involved active UC.
Project description:To further characterize the downstream targets of uc.323, we performed global microarray analysis after knockdown of uc.323 in cardiomyocytes to gain broad insight into uc.323-mediated transcriptome changes.
Project description:Activation of inflammatory pathways in human IBD. Leukocyte recruitment pathways including those for eosiniphils are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory eotaxin (CCL11) dependent networks would be up regulated in the colon of pediatric patients with Ulcerative Colitis (UC), and that these would regulate eosinophil recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Colon biopsy samples were obtained from UC patients at diagnosis, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that a leukocyte recruitment network which includeds CCL11 is up regulated in pediatric UC at diagnosis. The degree of up regulation of these genes compared to healthy controls was remarkably conserved within the UC patient group, suggesting common mechanisms of mucosal inflammation. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Keywords: Single time point in UC and healthy controls. Colon RNA was isolated from biopsies obtained from UC at diagnosis and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1,2,4,5) used for ormalization of the Sample VALUEs are also contained within this data set.
Project description:Activation of inflammatory pathways in human IBD. Leukocyte recruitment pathways including those for eosiniphils are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory eotaxin (CCL11) dependent networks would be up regulated in the colon of pediatric patients with Ulcerative Colitis (UC), and that these would regulate eosinophil recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Colon biopsy samples were obtained from UC patients at diagnosis, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that a leukocyte recruitment network which includeds CCL11 is up regulated in pediatric UC at diagnosis. The degree of up regulation of these genes compared to healthy controls was remarkably conserved within the UC patient group, suggesting common mechanisms of mucosal inflammation. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Keywords: Single time point in UC and healthy controls.
Project description:Ulcerative colitis (UC), a chronic, nonspecific inflammatory bowel disease characterized by continuous and diffuse inflammatory changes in the colonic mucosa, requires novel treatment method. Photodynamic therapy (PDT), as a promising physico-chemical treatment method, were used to treat UC rats’ model with novel photosensitizer LD4 in this paper, the treatment effect and mechanism was investigated. LD4-PDT could improve the survival rate of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced UC model rats, decrease expression of interleukin (IL)-6, IL-1, tumor necrosis factor (TNF)-α, malondialdehyde (MDA), myeloperoxidase (MPO) and increase the expression of glutathione (GSH) and superoxide oxidase (SOD), while protecting the integrity of the intestinal epithelium. LD4-PDT treatment could rebuild the intestinal microflora composition and reprogram the colonic protein profiles in TNBS-induced rats to almost the normal state. Proteomics analysis based upon TNBS-induced UC model rats revealed that Amine oxidase copper-containing 1 (AOC1) was a potential target of LD4-PDT. Novel photosensitizer agent LD4-PDT represents an efficient treatment method for UC, and AOC1 may be a promising target.