Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA99205 | ENA |
REPOSITORIES: ENA
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Project description:Idiopathic pulmonary fibrosis (IPF), a chronic progressive lung disease of unknown etiology, is characterized by the expansion of myofibroblasts and abnormal deposition of extracellular matrix in the lung parenchyma. To elucidate the molecular mechanisms that lead to IPF, we analyzed myofibroblasts established from patients with IPF by oligonucleotide microarrays. Gene expression profiles revealed a novel pathophysiologic function of myofibroblasts as a generator of reactive oxygen species, and a self-defense mechanism against oxidative stress of their own generating. Experiment Overall Design: We isolated two myofibroblast cell culture from patients with idiopathic pulmonary fibrosis. Embryonic pulmonary fibroblast was used for the reference.
2008-06-15 | E-GEOD-6804 | biostudies-arrayexpress
Project description:miRNA expression data in idiopathic pulmonary fibrosis
| PRJNA109903 | ENA
Project description:MicroRNA expression data in Idiopathic Pulmonary Fibrosis
| PRJNA137221 | ENA
Project description:MicroRNA expression data from lung tissue of Idiopathic Pulmonary Fibrosis
| PRJNA304959 | ENA
Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease where invasive pulmonary myofibroblasts secrete collagen and destroy lung integrity. Here we show that IL-11 is upregulated in the lung of IPF patients, associated with disease severity and is secreted from IPF fibroblasts. In vitro, IL-11 stimulates lung fibroblasts to become invasive, ACTA2+ve, collagen secreting myofibroblasts, in an ERK-dependent fashion. In mice, fibroblast-specific transgenic expression or administration of Il-11 drives lung fibroblast-to-myofibroblast transformation and causes lung fibrosis. Il11ra1 deleted mice, whose lung fibroblasts are unresponsive to pro-fibrotic stimulation, are protected from fibrosis in the bleomycin mouse model of pulmonary fibrosis. We generated an IL-11 neutralising antibody that blocks lung fibroblast activation downstream of multiple stimuli and reverses myofibroblast activation. In therapeutic studies, anti-IL-11 treatment both prevented and reversed lung fibrosis, which was accompanied by diminished Erk activation. These data prioritise IL-11 as a drug target for lung fibrosis and IPF.
2022-05-06 | GSE130983 | GEO
Project description:The interaction of lung epithelial and lung mesenchymal cells was investigated in a novel co-culture model of human pulmonary fibrosis. Remarkably, co-culturing both cell types induced cell-type-specific responses, including fibroblast-to-myofibroblast differentiation and epithelial-to-mesenchymal transition (EMT), which were fully dependent on direct epithelial / fibroblast contact. We used single-cell RNA sequencing (scRNA-seq) to evaluate the transcriptional fate of the normal human lung fibroblasts (NHLF) and normal human bronchiolar epithelial cells (NHBE) during the course of co-cultivation, and compare the single cell profiles with their counterpart isolated from patients with idiopathic pulmonary fibrosis (IPF). NHLF and normal NHBE cells were grown as co-cultures, cell suspensions were collected at the time points t = 0h, 3h and 18h and analyzed by single-cell RNA-seq on a Chromium Platform. Eight samples were sequenced, resulting in a total of xx single cell transcription profiles.
2022-10-03 | E-MTAB-11847 | biostudies-arrayexpress
Project description:Validated Gene Expression Signatures of Idiopathic Pulmonary Fibrosis
| PRJNA130183 | ENA
Project description:Profiling of Gene Expression in Idiopathic Pulmonary Fibrosis
| PRJNA169421 | ENA
Project description:Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant accumulation of collagen-secreting myofibroblasts. Development of effective therapies is limited due to incomplete understanding of molecular mechanisms regulating myofibroblast expansion. FOXF1 transcription factor is expressed in resident lung fibroblasts, but its role in lung fibrosis remains unknown due to the lack of genetic mouse models. Through comprehensive analysis of human IPF genomics data, lung biopsies and transgenic mice with fibroblast-specific inactivation of FOXF1, the present study shows that FOXF1 inhibits pulmonary fibrosis. FOXF1 deletion increases myofibroblast invasion, collagen secretion, and promotes a switch from of N-cadherin (CDH2) to Cadherin-11 (CDH11), which is critical step in acquisition of pro-fibrotic phenotype. FOXF1 directly binds to Cdh2 and Cdh11 promoters and differentially regulates transcription of these genes. Re-expression of CDH2 or inhibition of CDH11 in FOXF1-deficient cells reduces myofibroblast invasion in vitro. FOXF1 inhibits pulmonary fibrosis by regulating a switch from CDH2 to CDH11 in lung myofibroblasts.
2018-08-09 | GSE110408 | GEO
Project description:Host-Microbial interactions in Idiopathic Pulmonary Fibrosis
| PRJNA361279 | ENA