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Expression profiles of immortal lung fibroblasts

ABSTRACT: Activation of telomerase often endows cancer cells, but rarely normal somatic cells, with immortality. Especially, fetal lung fibroblasts are known to be hardly immortalized by TERT overexpression. We here established an immortal non-transformed lung fibroblast cell line only by TERT transfection, as well as an immortal transformed cell line by transfection of TERT and SV40 early antigens. Comparing the expression profiles of these cell lines with those of mortal cell strains with elongated lifespan after TERT transfection, 51 genes, including 19 upregulated and 32 downregulated, were explored to be the candidates responsible for regulation of cellular proliferation of lung fibroblasts. These included the genes previously reported to be involved in cellular proliferation, transformation, or self-renewal capacity, and those highly expressed in lung tissues obtained from patients with idiopathic pulmonary fibrosis or hypersensitivity pneumonitis. This set of lung fibrobrast cell lines/strains of identical genetic background with different proliferative capacity, mortal and immortal non-transformed fibroblasts may become useful model cells for research on lung fibroblast growth regulation and the candidate genes explored in this study may provide promising biomarkers or molecular targets of pulmonary fibrosis. Keywords: Cell type comparison

ORGANISM(S): Homo sapiens

PROVIDER: GSE9077 | GEO | 2008/04/01

SECONDARY ACCESSION(S): PRJNA102595

REPOSITORIES: GEO

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Expression profiles of immortal lung fibroblasts

Project description:Activation of telomerase often endows cancer cells, but rarely normal somatic cells, with immortality. Especially, fetal lung fibroblasts are known to be hardly immortalized by TERT overexpression. We here established an immortal non-transformed lung fibroblast cell line only by TERT transfection, as well as an immortal transformed cell line by transfection of TERT and SV40 early antigens. Comparing the expression profiles of these cell lines with those of mortal cell strains with elongated lifespan after TERT transfection, 51 genes, including 19 upregulated and 32 downregulated, were explored to be the candidates responsible for regulation of cellular proliferation of lung fibroblasts. These included the genes previously reported to be involved in cellular proliferation, transformation, or self-renewal capacity, and those highly expressed in lung tissues obtained from patients with idiopathic pulmonary fibrosis or hypersensitivity pneumonitis. This set of lung fibrobrast cell lines/strains of identical genetic background with different proliferative capacity, mortal and immortal non-transformed fibroblasts may become useful model cells for research on lung fibroblast growth regulation and the candidate genes explored in this study may provide promising biomarkers or molecular targets of pulmonary fibrosis. Keywords: Cell type comparison We analyzed 6 arrays with Affymetrix, 4 arrays with Agilent, and 7 arrays with CodeLink oligonucleotide microarrays for lung fibroblasts with various lifespan with or without transfection of TERT and/or SV40 early antigens.

2010-05-22 | E-GEOD-9077 | biostudies-arrayexpress

Expression profiles of esophageal cancer cell lines

Project description:Expression profiles of immortal esophageal squamous cancer cell lines were compared with those of cultured mortal noncancerous esophageal epithelial cells. Keywords: Cell type comparison

2008-12-01 | GSE9982 | GEO

Expression data from fibroblasts cultured from normal and fibrotic human lung tissue

Project description:Pulmonary fibrosis develops as a consequence of environmentally induced lung injury and/or an inherent disease susceptibility causing fibroblast activation, proliferation and extracellular matrix deposition. The study was undertaken to characterise global gene expression in pulmonary fibroblasts to better understand the mechanisms underlying the fibrotic fibroblast phenotype. Gene expression was evaluated in lung fibroblasts derived from ten controls (normal periphery of resected tumor), open lung biopsies from eight patients with interstitial lung disease associated with systemic sclerosis (fibrotic non specific interstitial pneumonia pattern on biopsy), and from three patients with usual interstitial pneumonia. Lung fibroblasts were grown to confluence in DMEM with 10% fetal calf serum. At confluence, lung fibroblasts were serum-deprived for 44 hours in the presence of fibroblast growth medium with the addition of 0.1% bovine serum albumin (Sigma).

2013-08-05 | E-GEOD-40839 | biostudies-arrayexpress

IL-11 is a therapeutic target in idiopathic pulmonary fibrosis

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

Loss of Fas-signaling in pro-fibrotic fibroblasts impairs homeostatic fibrosis resolution and promotes persistent pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible fibrotic disease of the distal lung alveoli that culminates in respiratory failure and reduced lifespan. Unlike normal lung repair in response to injury, IPF is associated with the accumulation and persistence of fibroblasts and myofibroblasts and continued production of collagen and other extracellular matrix (ECM) components. Prior in vitro studies have led to the hypothesis that the development of resistance to Fas-induced apoptosis by lung fibroblasts and myofibroblasts contibributes to their accumulation in the distal lung tissues of IPF patients. Here, we test this hypothesis in vivo in the resolving model of bleomycin-induced pulmonary fibrosis in mice. Using genetic loss-of-function approaches to inhibit Fas signaling in fibroblasts, novel flow cytometry strategies to quantify lung fibroblast subsets and transcriptional profiling of lung fibroblasts by bulk and single cell RNA-sequencing, we show that Fas is necessary for lung fibroblast apoptosis during homeostatic resolution of bleomycin-induced pulmonary fibrosis in vivo. Furthermore, we show that loss of Fas signaling leads to the persistence and continued pro-fibrotic functions of lung fibroblasts. Our studies provide novel insights into the mechanisms that contribute to fibroblast survival, persistence and continued ECM deposition in the context of IPF and how failure to undergo Fas-induced apoptosis prevents fibrosis resolution.

2020-11-18 | GSE161648 | GEO

Microarray analysis of cell types exposed to alpha particle radiation

Project description:Four human-derived cell types: transformed monocytes (THP-1), transformed lung epithelial cells (A549), normal human pulmonary endothelial cells (HPEAC) and normal lung fibroblasts (HFL-1) Cell types were independently exposed to alpha particle radiation using Americium-241 discs (0.9Gy/hr) at a dose range from 0-1.5 Gy. Twenty-four hours post-exposure cells were harvested and RNA was extracted and subjected to microarray analysis.

2016-05-04 | GSE81067 | GEO

Expression data from fibroblasts cultured from normal and fibrotic human lung tissue

2013-08-05 | GSE40839 | GEO

Gene expression in lung fibroblasts

Project description:Pulmonary fibrosis is a chronic, progressive, and lethal interstitial lung disease. It is characterized by extracellular matrix deposition, fibroblast proliferation, and accumulation. Fibroblasts from normal or UIP histology were cultured and analyzed. Keywords: Fibroblasts from normal histology lung tissue or UIP histology lung tissue

2009-03-19 | GSE10921 | GEO

Forkhead Box F1 (FOXF1) represses fibroblast functions relevant to fibrogenesis

Project description:Aberrant expression of master phenotype regulators by lung fibroblasts may play a central role in idiopathic pulmonary fibrosis (IPF). Interrogating IPF fibroblast transcriptome datasets, we identified Forkhead Box F1 (FOXF1), a DNA-binding protein required for lung development, as a candidate actor in IPF. Thus, we determined FOXF1 expression levels in fibroblasts cultured from normal or IPF lungs in vitro, and explored FOXF1 functions in these cells using transient and stable loss-of-function and gain-of-function models. FOXF1 mRNA and protein were expressed at higher levels in IPF compared with controls. In normal lung fibroblasts, FOXF1 repressed key fibroblast functions such as proliferation, survival, and expression of collagen-1 (COL1) and actin related protein 2/3 complex, subunit 2 (ARPC2). ARPC2 knockdown mimicked FOXF1 overexpression with regard to proliferation and COL1 expression. FOXF1 expression was induced by the antifibrotic mediator prostaglandin E2 (PGE2). Ex vivo, FOXF1 knockdown conferred CCL-210 lung fibroblasts the ability to implant and survive in uninjured mouse lungs. In IPF lung fibroblasts, FOXF1 regulated COL1 but not ARPC2 expression. In conclusion, FOXF1 functions and regulation were consistent with an antifibrotic role in lung fibroblasts. Higher FOXF1 levels in IPF fibroblasts may thus participate in a compensatory response to fibrogenesis. Lung fibroblasts derived from 4 different IPF patients (P313, P355, P375 and P426) were transiently transfected with pcfoxf1 or control pcDNA3.1-constructs. Total RNAs were extracted 24 h after transfection and hybridized on microarrays. One color experiment with 2 experimental conditions: pcfoxf1 and pcDNA3.1

2014-10-01 | E-GEOD-52612 | biostudies-arrayexpress

RNA-seq time series of lung epithelial and lung mesenchymal cells in a novel co-culture model of lung fibrosis

Project description:The interaction of lung epithelial and lung mesenchymal cells (fibroblasts) 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. Primary normal human lung fibroblasts (NHLF) and normal human bronchiolar epithelial cells (NHBE) were fluorescently labelled prior to seeding, then grown either as mono or co-cultures and collected in triplicates for mRNA-seq at the start (T=0h) and after 3h and 18h. Each harvested cell culture was FACS sorted into individual NHLF and NHBE cell populations, which were then then lysed and sequenced.

2022-10-03 | E-MTAB-11832 | biostudies-arrayexpress

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