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Identification of microRNA expression patterns in human myofibroblasts with/without the JQ-1 treatment and/or TGF-b

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease that normal parenchyma is progressively replaced by fibrotic foci comprised of myofibroblasts, active differentiated fibroblasts. IPF has an overall poor prognosis with median survival ranging from 2.5 to 3.5 years. The underlying disease mechanisms in IPF are largely unknown, and there is still no effective drug that prolongs survival of patients with IPF. It has been known that JQ-1, a BET bromodomain inhibitor, prevents TGF-β-mediated fibroblast to myofibroblast differentiation. Moreover, JQ-1 modulates miRNAs expression in various types of cancer cell. In this study, to gain understanding of the relationship between miRNAs expression and the effect of JQ-1 on the dedifferentiation of established myofibroblast, we investigated miRNA profiles in human myofibroblasts with/without the JQ-1 treatment and/or TGF- using miRNA microarray assay.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE140475 | GEO | 2020/07/11

REPOSITORIES: GEO

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Project description:As a group, fibroproliferative disorders of the lung, liver, kidney, heart, vasculature and integument are common, progressive and refractory to therapy. They can emerge following toxic insults, but are frequently idiopathic. Their enigmatic propensity to resist therapy and progress to organ failure has focused attention on the myofibroblast – the primary effector of the fibroproliferative response. A central unanswered question is whether these myofibroblasts have acquired a distinct pathological phenotype - or whether they are normal myofibroblasts with a pathological phenotype that depends upon residing in a sea of pro-fibrotic cytokines and an abnormal extracellular matrix. Using a systems approach to study this question in a prototype fibrotic disease, Idiopathic Pulmonary Fibrosis (IPF); here we show organized changes in the gene expression pathway of primary lung myofibroblasts that persist for up to 9 sub-cultivations in vitro. When comparing IPF and control myofibroblasts in a 3-dimensional type I collagen matrix, more genes differed at the level of ribosome recruitment than at the level of transcript abundance, indicating pathological translational control as a major characteristic of IPF myofibroblasts. To determine the effect of matrix state on translational control, myofibroblasts were permitted to contract the matrix. Ribosome recruitment in control myofibroblasts was relatively stable. In contrast, IPF cells manifested large alterations in the ribosome recruitment pattern. Pathological studies suggest an epithelial origin for IPF myofibroblasts through the epithelial to mesenchymal transition (EMT). In accord with this, we found systems-level indications for TGF?b -driven EMT as one source of IPF myofibroblasts. Keywords: cell type comparison Comparison of lung myofibroblasts from patients with Idiopatic Pulmonary Fibrosis (IPF, 6 donors) to control (6 donors) in contractile and non-contractile matrices using both total and polyribosomal RNA

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Identification of microRNA expression patterns in human myofibroblasts with/without the JQ-1 treatment and/or TGF-b

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