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Genome-wide DNA Methylation Analysis in Lung Fibroblasts Co-cultured with Silica-exposed Alveolar Macrophages

ABSTRACT: In the present study, we used MeDIP coupled with next-generation sequencing to profile the whole genome DNA methylation patterns of fibroblast from the co-culture model in vitro. We analyzed the data to identify possible biological pathways for fibroblast differentiating into myofibroblast as well as the interactions of related genes.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE93116 | GEO | 2017/01/04

SECONDARY ACCESSION(S): PRJNA360081

REPOSITORIES: GEO

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Genome-wide DNA methylation analysis in lung fibroblasts co-cultured with silica-exposed alveolar macrophages.

Project description:BackgroundExposure to crystalline silica is considered to increase the risk of lung fibrosis. The primary effector cell, the myofibroblast, plays an important role in the deposition of extracellular matrix (ECM). DNA methylation change is considered to have a potential effect on myofibroblast differentiation. Therefore, the present study was designed to investigate the genome-wide DNA methylation profiles of lung fibroblasts co-cultured with alveolar macrophages exposed to crystalline silica in vitro.MethodsAM/fibroblast co-culture system was established. CCK8 was used to assess the toxicity of AMs. mRNA and protein expression of collagen I, α-SMA, MAPK9 and TGF-β1 of fibroblasts after AMs exposed to 100 μg /ml SiO2 for 0-, 24-, or 48 h were determined by means of quantitative real-time PCR, immunoblotting and immunohistochemistry. Genomic DNA of fibroblasts was isolated using MeDIP-Seq to sequence. R software, GO, KEGG and Cytoscape were used to analyze the data.ResultsSiO2 exposure increased the expression of collagen I and α-SMA in fibroblasts in co-culture system. Analysis of fibroblast methylome identified extensive methylation changes involved in several signaling pathways, such as the MAPK signaling pathway and metabolic pathways. Several candidates, including Tgfb1 and Mapk9, are hubs who can connect the gene clusters. MAPK9 mRNA expression was significantly higher in fibroblast exposed to SiO2 in co-culture system for 48 h. MAPK9 protein expression was increased at both 24-h and 48-h treatment groups. TGF-β1 mRNA expression of fibroblast has a time-dependent manner, but we didn't observe the TGF-β1 protein expression.ConclusionTgfb1 and Mapk9 are helpful to explore the mechanism of myofibroblast differentiation. The genome-wide DNA methylation profiles of fibroblasts in this experimental silicosis model will be useful for future studies on epigenetic gene regulation during myofibroblast differentiation.

| S-EPMC5429546 | biostudies-literature

LKB1 inhibition in alveolar epithelial cells induces fibroblast activation in pulmonary fibrosis [RNA-seq in 3D co-cultured ATII+MRC5]

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, and lethal lung disease. The initiation of IPF involves microinjuries to and/or dysfunction of the alveolar epithelium, but factors that determine fibrosis progression or normal tissue repair are largely unknown. We previously demonstrated that autophagy inhibition-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments local myofibroblast differentiation in pulmonary fibrosis by paracrine signalling. Here, we report that liver kinase B1 (LKB1) inactivation in ATII cells induces autophagy inhibition and EMT as a consequence. In IPF lungs, this is caused by a downregulation of CAB39L, a key subunit within the LKB1 complex. 3D co-cultures of ATII cells and lung fibroblast MRC5 coupled with RNA sequencing (RNA-seq) confirmed that paracrine signalling between LKB1-depleted ATII cells and fibroblasts augmented myofibroblast differentiation. Together these data suggest that reduced autophagy caused by LKB1 inhibition can induce EMT in ATII cells and contribute to fibrosis via aberrant epithelial–fibroblast crosstalk.

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LKB1 inhibition in alveolar epithelial cells induces fibroblast activation in pulmonary fibrosis [RNA-seq in 2D-cultured ATII]

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Effect of PLX4720 on melanoma-associated fibroblasts co-cultured with melanoma cells

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Effect of PLX4720 on melanoma-associated fibroblasts co-cultured with melanoma cells

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Effect of PLX4720 on melanoma cells co-cultured with melanoma-associated fibroblasts

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Transcriptome analysis of primary airway epithelial cells co-cultured with human lung fibroblasts

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Comparative analysis of co-cultured amniotic cell conditioned media with cell-free amniotic fluid

Project description:Myofibroblast activation is a cellular response elicited by a variety of physiological or pathological insults whereby cells initiate a coordinated response intended to eradicate the insult and then revert back to a basal state. However, an underlying theme in various disease states is persistent myofibroblast activation that fails to resolve. Based on multiple observations, we hypothesized that the secreted factors harvested from co-culturing amniotic stem cells might mimic the anti-inflammatory state that cell-free amniotic fluid (AF) elicits. We optimized an amnion epithelial and amniotic fluid cell co-culture system, and tested this hypothesis in the context of myofibroblast activation. However, we discovered that co-cultured amniotic cell conditioned media (coACCM) and AF have opposing effects on myofibroblast activation: coACCM activates the epithelial-mesenchymal transition (EMT) and stimulates gene expression patterns associated with myofibroblast activation, while AF does the opposite. Intriguingly, purified extracellular vesicles (EVs) from AF are necessary and sufficient to activate EMT and inflammatory gene expression patterns, while the EV-depleted AF potently represses these responses. In summary, these data indicate that coACCM stimulates myofibroblast activation, while AF represses it. We interpret these findings to suggest that coACCM, AF, and fractionated AF represent unique biologics that elicit differential cellular responses correlated with a wide variety of pathological states, and therefore could have broad utility in the clinic and the lab.

2022-08-19 | MSV000090160 | MassIVE

ADAMTS12 serves as a checkpoint in fibrosis that controls migration and expansion of injury-responsive fibroblasts

Project description:Fibrosis represents the uncontrolled replacement of parenchymal tissue with extracellular matrix (ECM) produced by myofibroblasts. While genetic fate-tracing and single-cell RNA-sequencing (scRNA-seq) technologies have helped elucidate fibroblast heterogeneity and ontogeny beyond fibroblast to myofibroblast differentiation, the novel identified fibroblast populations remain ill-defined, both in respect to the molecular cues driving their differentiation, and their subsequent role in fibrosis. Here we identify the metalloprotease ADAMTS12 in an unbiased manner as a fibroblast-specific gene that is strongly upregulated during fibrogenesis in mice and humans. In vivo knockout studies in mice confirmed that Adamts12 is critical during fibrogenesis in heart and kidney. Leveraging spatial transcriptomics, CRISPR-Cas9 gene editing and expression of catalytically active or inactive ADAMTS12 we demonstrate that the protease domain of Adamts12 controls fibrogenesis by licensing expansion and migration of a distinct fibroblast subset defined by Mt1 gene expression and strong JAK-STAT signaling.

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