Skip to main content
Fig. 3 | BMC Medical Genomics

Fig. 3

From: Glucocorticoid-driven transcriptomes in human airway epithelial cells: commonalities, differences and functional insight from cell lines and primary cells

Fig. 3

Genes induced by budesonide in A549, BEAS-2B and primary human bronchial epithelial (HBE) cells. A549 (N = 3), BEAS-2B (N = 4), and primary HBE (N = 4 donors) cells were not treated or treated with budesonide (300 nM for A549 and BEAS-2B, 100 nM for HBE) for 6 h. RNA was prepared, and microarray analysis performed using Affymetrix Primeview arrays. Probe set intensities from the different samples were normalized using the robust multi-array average (RMA) method. Comparing the probe set intensities of the treated samples against their untreated controls identified 410 genes showing significant induction ≥2 fold (P ≤ 0.05) compared to untreated control in any of the cell variants (Additional file 5). a. The genes meeting these criteria in each cell variant were used to produce a Venn diagram to illustrate commonality between the three cell variants. The 17 genes induced in common were subjected to GO analysis in DAVID and are shown along with GO terms showing significant enrichment (EASE score ≤ 0.1) with genes from this list. Genes representing each term are indicated. GO terms are categorized into 3 primary groups (transcription, proliferation/apoptosis or signaling) as indicated. b. The 410 genes were then grouped as defined by the lower stringency, ≥ 1.25 fold, cut-off (Additional file 5). The genes within each group are listed in Additional file 5. Heat maps were constructed for each grouping. Data are presented as zero-mean log2 intensity, centered around the mean of untreated (not stimulated; NS) and treated for each gene in each cell variant. Following GO analysis in DAVID, GO terms, showing significant enrichment (EASE score ≤ 0.1) and representing at least 5 genes of the 93 genes induced in common, are listed. The number of genes associated with each term are indicated. The GO terms were then categorized into 3 primary groups (transcription, proliferation/apoptosis or signaling), or other, as shown

Back to article page