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Gene expression signatures for MMP19 full length cDNA transfection in A549 cells.

ABSTRACT: To further understand the role of MMP19 in IPF, particularly in genotype and phenotype changes, we have employed whole genome microarray expression profiling as a discovery platform to identify the target genes of MMP19 in epithelial cells. Gene expression analysis showed that 8358 genes were differentially expressed at p-value 0.05 level and 748 genes were significantly changed with MMP19 expression, which covers matrix protien and cell proliferation, motality and phenotype changes (EMT). Among them, PTGS2 was revealed as one of the most significantly up-regulated genes. And PTGS2 up-regulation in IPF lungs was verified by immunohistochemical (IHC), qRT-PCR and Western-blot as well.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34994 | GEO | 2013/01/11

SECONDARY ACCESSION(S): PRJNA159575

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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Gene expression signatures for MMP19 full length cDNA transfection in A549 cells.

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