Figure 7
Cells with PPARγ mutation have an impaired PPARγ response. (A-B) Microarray transcript profiles are shown for selected probe sets that were induced (A) or repressed (B) in normal DCs (24 hours cells) upon PPARγ ligand treatment. Data were normalized to the median expression. Data were obtained from normal (3 DC samples) and mutated cells (C114R, R357X). As a further control, microarray data were also obtained from a patient with insulin resistance (IR). Cells were cultured for 24 hours and treated with 1 μM rosiglitazone (RSG). (C,D) TLDA analyses of selected up- (C) or down-regulated (D) genes of normal and mutated cells (C114R, R357X). qRT-PCR data were normalized to PPARγ ligand–treated normal DCs (WT RSG) and dendograms were obtained from hierarchical clustering (standard correlation). On the top of the dendograms the percentage of genes significantly (changes were at least 1.5-fold and P < .05) up- or down-regulated is indicated compared with normal (WT RSG) DCs.

Cells with PPARγ mutation have an impaired PPARγ response. (A-B) Microarray transcript profiles are shown for selected probe sets that were induced (A) or repressed (B) in normal DCs (24 hours cells) upon PPARγ ligand treatment. Data were normalized to the median expression. Data were obtained from normal (3 DC samples) and mutated cells (C114R, R357X). As a further control, microarray data were also obtained from a patient with insulin resistance (IR). Cells were cultured for 24 hours and treated with 1 μM rosiglitazone (RSG). (C,D) TLDA analyses of selected up- (C) or down-regulated (D) genes of normal and mutated cells (C114R, R357X). qRT-PCR data were normalized to PPARγ ligand–treated normal DCs (WT RSG) and dendograms were obtained from hierarchical clustering (standard correlation). On the top of the dendograms the percentage of genes significantly (changes were at least 1.5-fold and P < .05) up- or down-regulated is indicated compared with normal (WT RSG) DCs.

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