Most kidney allograft losses are caused by chronic allograft dysfunction (CAD). The aim of the study was to correlate changes in gene expression over time during the development of chronic damage in contrast to13cisRA Treated animal that demonstrated morphologically healthy kidneys by the end of teh study. Renal allografts were harvested from placebo and13cisRA Treatment groups for time points 0d, 7d, 14d and 56d (n=3-5) and examined for steady state mRNA expression using Affymetrix microarray RG-U34A. The effect of the13cisRA Treatment on dysregulated pathways was examined. In order to verify the microarray analysis, qPCR has been performed.
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Specimen part
View SamplesMost kidney allograft losses are caused by chronic allograft dysfunction (CAD) that is characterized by interstitial fibrosis, tubular atrophy and a smoldering inflammatory process. The aim of the study was to correlate changes in gene expression over time, as evidenced by effects on regulatory pathways linked to the development of fibrosis and inflammation during the development of chronic damage. Renal allografts were harvested for time points 0d, 7d, 14d and 56d (n=3-5) and examined for steady state mRNA expression using Affymetrix microarray RG-U34A. A select group of genes previously associated with chronic fibrosis was then examined in the context of progressive dysfunction. In order to verify the microarray analysis, qPCR has been performed.
Wnt pathway regulation in chronic renal allograft damage.
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View SamplesWe found various genes involved in differentiation (RGMB, LRRC17), cell cycle control (Cyclin E1) and apoptosis (LIMA1, CAMK2N1) were found to be deregulated in osteosarcoma cell lines, most likely due to altered miRNA expression patterns.
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Specimen part, Cell line
View SamplesExperimental autoimmune uveitis (EAU) in Lewis rats is a model for the clinical heterogeneity of human uveitis. The autoantigens inducing disease in the rat are also seen in human disease. Depending upon the specific autoantigen used, the experimental disease course can be either monophasic or relapsing/remitting and appears to be dictated by the T cell effector phenotype elicited. We investigated potential differences between monophasic and relapsing/remitting effector T cells using transcriptomic profiling and pathway analysis. RNA samples isolated from three independent T cell lines derived from each specificity where analyzed by microarrays.
Effector T cells driving monophasic vs. relapsing/remitting experimental autoimmune uveitis show unique pathway signatures.
Specimen part
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