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Gene expression profiling in blood of patients with chronic respiratory failure

ABSTRACT: Genes dysregulated in cystic fibrosis (CF) and primary pulmonary arterial hypertension (PAH) at a late stage of pulmonary failure are still largely unknown. Blood samples taken in the frame of the French cohort of lung transplantation COLT offers the opportunity to identify in blood specific gene signatures of each disease and a common gene signature for both pathologies. A microarray analysis was performed with homogeneous groups of CF patients (n=23), PAH (n=13) patients and healthy volunteers (n=28). Blood was collected in a PAXgene® tube to maintain RNA integrity. Total extracted RNA were processed on 60K whole-genome microarrays (Agilent Technologies). Microarrays were analyzed by bioinformatics (GOminer and Ingenuity Pathway Analysis). Three major biological signatures were discovered including (1) genes specifically over-expressed in pPAH and mainly involved in inflammation, vascular remodeling and cell proliferation, (2) genes specifically over-expressed in CF involved in innate immune response and oxidative stress response, and (3) genes under-expressed in both diseases, including genes involved in transcriptional machinery, apoptosis and cell proliferation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38267 | GEO | 2014/12/09

SECONDARY ACCESSION(S): PRJNA167505

REPOSITORIES: GEO

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Project description:Objective: Pulmonary complications in systemic sclerosis (SSc), including pulmonary fibrosis (PF) and pulmonary arterial hypertension (PAH), are the leading cause of mortality. We compared the molecular fingerprint of SSc lung tissues and matching primary lung fibroblasts to those of normal donors, and patients with idiopathic pulmonary fibrosis (IPF) and idiopathic pulmonary arterial hypertension (IPAH). Methods: Lung tissues were obtained from 33 patients with SSc who underwent lung transplantation. Tissues and cells from a subgroup of SSc patients with predominantly PF or PAH were compared to those from normal donors, patients with IPF, or IPAH. Microarray data was analyzed using Efficiency Analysis for determination of optimal data processing methods. Real time PCR and immunohistochemistry were used to confirm differential levels of mRNA and protein, respectively. Results: We identified a consensus of 242 and 335 genes that were differentially expressed in lungs and primary fibroblasts, respectively. Enriched function groups in SSc-PF and IPF lungs included fibrosis, insulin-like growth factor signaling and caveolin-mediated endocytosis. Functional groups shared by SSc-PAH and IPAH lungs included antigen presentation, chemokine activity, and IL-17 signaling. Conclusion: Using microarray analysis on carefully phenotyped SSc and comparator lung tissues, we demonstrated distinct molecular profiles in tissues and fibroblasts of patients with SSc-associated lung disease compared to idiopathic forms of lung disease. Unique molecular signatures were generated that are disease- (SSc) and phenotype- (PF vs PAH) specific. These signatures provide new insights into pathogenesis and potential therapeutic targets for SSc lung disease. Lung tissues were obtained from 33 patients with SSc who underwent lung transplantation. Tissues and cells from a subgroup of SSc patients with predominantly PF or PAH were compared to those from normal donors, patients with IPF, or IPAH. Microarray data was analyzed using Efficiency Analysis for determination of optimal data processing methods. Real time PCR and immunohistochemistry were used to confirm differential levels of mRNA and protein, respectively.

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Gene expression profiling in blood of patients with chronic respiratory failure

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