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Gene expression analysis of normal primary human bronchial epithelial cells (pHBEC) stimulated by glucocorticoid, long-acting β2-adrenoceptor agonist or both combined.

ABSTRACT: Gene expression analysis of normal primary human bronchial epithelial cells (pHBEC) stimulated by glucocorticoid, long-acting β2-adrenoceptor agonist or both combined.

PROVIDER: PRJNA679552 | ENA |

REPOSITORIES: ENA

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Gene expression analysis of normal primary human bronchial epithelial cells (pHBEC) stimulated by glucocorticoid, long-acting β2-adrenoceptor agonist or both combined.

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Gene expression analysis of human bronchial airway epithelial BEAS-2B cells stimulated by glucocorticoid, long-acting β2-adrenoceptor agonist or both combined.

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A comparison of GS-5759, a bifunctional β2-adrenoceptor agonist and PDE4 inhibitor, and indacaterol and GSK 256066 in combination on gene expression changes in the BEAS-2B human airway epithelial cell line

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The long-acting β2 -adrenoceptor agonist, indacaterol, enhances glucocorticoid receptor-mediated transcription in human airway epithelial cells in a gene- and agonist-dependent manner.

Project description:Background and purposeInhaled glucocorticoid (ICS)/long-acting β2 -adrenoceptor agonist (LABA) combination therapy is a recommended treatment option for patients with moderate/severe asthma in whom adequate control cannot be achieved by an ICS alone. Previously, we discovered that LABAs can augment dexamethasone-inducible gene expression and proposed that this effect may explain how these two drugs interact to deliver superior clinical benefit. Herein, we extended that observation by analysing, pharmacodynamically, the effect of the LABA, indacaterol, on glucocorticoid receptor (GR)-mediated gene transcription induced by seven ligands with intrinsic activity values that span the spectrum of full agonism to antagonism.Experimental approachBEAS-2B human airway epithelial cells stably transfected with a 2× glucocorticoid response element luciferase reporter were used to model gene transcription together with an analysis of several glucocorticoid-inducible genes.Key resultsIndacaterol augmented glucocorticoid-induced reporter activation in a manner that was positively related to the intrinsic activity of the GR agonist. This effect was demonstrated by an increase in response maxima without a change in GR agonist affinity or efficacy. Indacaterol also enhanced glucocorticoid-inducible gene expression. However, the magnitude of this effect was dependent on both the GR agonist and the gene of interest.Conclusions and implicationsThese data suggest that indacaterol activates a molecular rheostat, which increases the transcriptional competency of GR in an agonist- and gene-dependent manner without apparently changing the relationship between fractional GR occupancy and response. These findings provide a platform to rationally design ICS/LABA combination therapy that is based on the generation of agonist-dependent gene expression profiles in target and off-target tissues.

| S-EPMC4409912 | biostudies-literature

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