Project description:The fetal human lung fibroblasts (MRC5) and primary adult human lung mesenchyme (AHLM) have different capabilities in supporting human alveolar type 2 cell transdifferentiation into basal KRT5+ cells.Therefore, we examined the transcriptome of AHLM vs. MRC5 by bulk RNAseq.
Project description:The purpose of this study was to examine the role of MAVS, ZBP1 and RIPK3 in the phenotype that develops when ADAR1 activity is impaired, in particular when the Za domain of ADAR1 is mutated. Mice homozygous for a Za domain-mutant allele of Adar1 (Adar1mZa/mZa mice) and mice carrying one mZa and one null Adar1 allele (Adar1-/mZa mice) were compared with control mice that were either wild type or heterozygous for the Adar1 mZa allele (Adar1wt/mZa mice). The effects of MAVS deficiency, RIPK3 deficiency, ZBP1 deficiency or ZBP1 Za domain mutations were assessed by analysing compound mutant mice. Given the early postnatal lethal phenotype that develops in Adar1-/mZa mice, comparisons were made in RNA isolated from lung tissue from newborn mice of each genotype (5 mice per genotype). As Adar1-/mZa mice additionally lacking Mavs or Zbp1 are viable, adult mice (15-20 weeks of age) were also used for several compound mutations as donors of lung tissue.
Project description:Pulmonary fibrosis (PF) is both an independent disease and a pathologic basis for fibroproliferative lung diseases. Understanding of underlying mechanisms of PF is critical for developing effective therapeutics. Fibroblasts activation and extracellular matrix deposition are critical in pathogenesis of PF. Stimulation of certain factors can induce profibrotic changes in fibroblasts. Evaluation of associated genes in treated fibroblasts is helpfu to analyze the profibrotic changes of this critical effector cell for PF. We used microarrays to detail the global programme of gene expression following TGFβ and CCL1 stimulation of primary lung fibroblasts.