Project description:Purpose: To elucidate the effects of SCD1 inhibitor in allergic airway inflammation. Method: Wild-type mice were sensitized intratracheally twice with house dust mite (HDM) extract at a 7-day interval. Along with that, an SCD-1 inhibitor, A939572 was also administered intraperitoneally daily. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 385 transcripts showed differential expression between SCD1 inhibitor-treated mice and DMSO (vehicle)-treated mice with adjusted p value <0.05.
Project description:Purpose: To elucidate the roles of airway epithelial STAT3 in allergic airway inflammation. Method: Doxycycline-induced airway epithelial cells-specific STAT3-deficient mice (STAT3-cKO) and their genetic control mice (STAT3-WT) were sensitized intratracheally twice with house dust mite (HDM) extract or PBS at a 7-day interval. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 206 transcripts showed differential expression between HDM-treated STAT3-WT and STAT3-cKO with adjusted p value <0.05.
Project description:The aim of this study was to investigate differential expression in a house dust mite (HDM) exposure model of asthma in rhesus macaques. HDM sensitization was performed by subcutaneous injection of HDM followed by intranasal HDM for 2-3 hours twice a week. Animals were mock-sensitized (PBS) or sensitized to HDM antigen. Gene expression was measured in lung biopsies before and fifteen weeks after treatment.
Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples.
Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples. Four established ccRCC cell lines purchased from ATCC were treated with DMSO control versus A939572 over a 24 hour time period. RNA from each group was isolated and sent of for gene array anaylsis. Gene expression data from each individual treatment group was normalized to its respective DMSO contol, and resulting expression patterns associated with drug exposure was compared between the four cell lines.
Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.
Project description:Quantitative proteomics in DIA mode was used to analysis the proteomic profile of 24 weeks from the sorafenib treated and vehicle treated monkeys.
Project description:We compared the transcriptomes of mesenchymal cells and immune cells in mice sensitized and challenged with house dust mite (HDM) extracts and those in control PBS-treated mice, using single cell RNA-seq (scRNA-seq). Data with mesenchymal cells and data with immune cells were obtained from separate experiments. For scRNA-seq of mesenchymal cells, each sample was pooled from cells from 3 mice and 2 different samples per group (for a total of 6 mice) were used. For scRNA-seq of immune cells, each sample was from cells of one individual mouse.