Project description:Whole transcriptional analysis of normal 16HBE14o- cells, cystic fibrosis (CF) patients-derived CFBE41o- cells, and WT-CFTR-rescued CFBE41o- cells. We utilized the gene expression data to understand the transcriptional regulation underlying the loss of CFTR function.
Project description:The purpose of this study was to explore baseline expression of miRNome in Cystic Fibrosis Bronchial Epithelial (CFBE41o-) cells stably transfected with wild type (WT) Cystic Fibrosis Transmembrane Conductance regulator (CFTR) and F508del-CFTR. To fulfill this goal miRNA sequencing was done to see miRNA landscape in CFBE41o- Cells with homozygous F508del mutated CFTR and in CFBE41o- Cells with homozygous WT-CFTR, without any treatment condition.
Project description:In the clinical setting, mutations in the CFTR gene enhance the inflammatory response to P. aeruginosa (PA01) infection, but measurements of the inflammatory response to pathogen stimulation by isolated airway epithelia can yield variable results. In this series, we exposed CFBE41o- cells over-expressing ∆F508/∆F508 CFTR and CFBE41o- cells rescued with wt-CFTR to P. aeruginosa biofilms. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL2, CXCL3, CXCR4 and TNF-α) in CFBE-wt-CFTR cells compared to CFBE-∆F508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o- ∆F508/∆F508-CFTR cells.
Project description:In the clinical setting, mutations in the CFTR gene enhance the inflammatory response to P. aeruginosa (PA01) infection, but measurements of the inflammatory response to pathogen stimulation by isolated airway epithelia can yield variable results. In this series, we exposed CFBE41o- cells over-expressing ?F508/?F508 CFTR and CFBE41o- cells rescued with wt-CFTR to P. aeruginosa biofilms. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL2, CXCL3, CXCR4 and TNF-?) in CFBE-wt-CFTR cells compared to CFBE-?F508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o- ?F508/?F508-CFTR cells. CFBE41o- cells generously provided by Dr. J.P. Clancy (University of Alabama). The series involved 4 treatment groups: unexposed wild type CFTR cells, unexposed ?F508/?F508 CFTR cells, wild type CFTR cells exposed to PA01, and ?F508/?F508 CFTR cells exposed to PA01. Each treatment group involved 4 replicate polarized monolayers. PAO1 was added to the apical side of exposed monolayers at a multiplicity of infection (MOI) of 30:1 for 1 hour in the absence of antibiotics, and then planktonic PAO1 was removed by replacing the apical medium with MEM supplemented with 0.4% arginine (2). Control monolayers were treated identically except that vehicle only (medium used to grow PAO1, MEM supplemented with 0.4% arginine) was added to the apical side of cells. Five hours after washing planktonic P. aeruginosa from the cell monolayers mRNA was isolated.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:Cystic fibrosis bronchial epithelial (CFBE41o-ΔF508) cells subjected to 23 bio-active small molecules including vehicle controls, at low temperature and untreated cells. Untreated Cystic fibrosis bronchial epithelial cells (CFBE41o−CFTR) are also included.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6