Leuenbergeria bleo
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA416167 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6269778_1.fastq.gz | Fastqsanger.gz | |||
| SRR6269778_2.fastq.gz | Fastqsanger.gz |
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Project description:Disease-Specific Gene Expression Profiling in Multiple Models of Lung Disease We profiled lung gene expression in 12 mouse models of infection, allergy, and lung injury. A total of 24 transcripts, including many involved in inflammation and immune activation, were differentially expressed in a substantial majority (9 or more) of the models. Expression patterns distinguished three groups of models: (1) bacterial infection (n = 5), with changes in 89 transcripts, including many related to nuclear factor-B signaling, cytokines, chemokines, and their receptors; (2) bleomycin-induced diseases (n = 2), with changes in 53 transcripts, including many related to matrix remodeling and Wnt signaling; and (3) T helper cell type 2 (allergic) inflammation (n = 5), with changes in 26 transcripts, including many encoding epithelial secreted molecules, ion channels, and transporters.
2006-12-31 | GSE4231 | GEO
Project description:Understanding the molecular underpinnings of cancer is of critical importance to developing targeted intervention strategies. Identification of such targets, however, is notoriously difficult and unpredictable. Malignant cell transformation requires the cooperation of a few oncogenic mutations that cause substantial reorganization of many cell features and induce complex changes in gene expression patterns. Genes critical to this multi-faceted cellular phenotype thus only have been identified following signaling pathway analysis or on an ad hoc basis. Our observations that cell transformation by cooperating oncogenic lesions depends on synergistic modulation of downstream signaling circuitry suggest that malignant transformation is a highly cooperative process, involving synergy at multiple levels of regulation, including gene expression. Here we show that a large proportion of genes controlled synergistically by loss-of-function p53 and Ras activation are critical to the malignant state. Remarkably, 14 among 24 such 'cooperation response genes' (CRGs) were found to contribute to tumor formation in gene perturbation experiments. In contrast, only one in 14 perturbations of genes responding in a non-synergistic manner had a similar effect. Synergistic control of gene expression by oncogenic mutations thus emerges as an underlying key to malignancy and provides an attractive rationale for identifying intervention targets in gene networks downstream of oncogenic gain and loss-of-function mutations. Experiment Overall Design: Contains 50 samples total, 10 replicates each of parental cell line YAMC, plus bleo/Neo vector control, mp53-expressing, Ras-expressing and mp53/Ras cells. Polysomal RNA from each sample was run on Affymetrix GeneChip® Mouse Genome 430 2.0 Arrays.
2008-06-18 | E-GEOD-9199 | biostudies-arrayexpress
Project description:Question addressed in the study: Genetic lineage tracing of alpha smooth muscle actin-positive (ACTA2+) cells in the context of bleomycin-induced pulmonary fibrosis in mice has shown that activated myofibroblasts (aMYFs) differentiate into lipofibroblasts (LIFs) during fibrosis resolution. However, the heterogeneity of the different mesenchymal cell subclusters during fibrosis formation and their contribution to the aMYFs as well as the fate of aMYFs during fibrosis resolution are still unclear. Materials and methods: Two-month-old Tg(Acta2-CreERT2); tdTomatoflox mice were used to label Acta2pos cells before (Tam-Bleo condition) or after (Bleo-Tam condition) bleomycin administration. Using scRNA-seq, the origin and fate of Acta2pos cells converging on the aMYF/Cthrc1pos myofibroblast lineage, were analyzed at the peak of fibrosis formation (day 14) as well as during resolution (day 60). Mining of human IPF scRNA-seq data was also carried out. The function of resident mesenchymal cells derived from saline or bleomycin-injured lungs during fibrosis formation or resolution in supporting AT2 progenitor cell renewal was assessed using alveolar organoid assays. Results: By employing the dimensionality reduction and UMAP visualization MYF/Cthrc1pos cells were identified and characterized in three scRNA-seq conditions: Saline, Tam-Bleo and Bleo-Tam. Acta2pos cells isolated from saline-treated mice revealed the presence of Acta2pos cells in the expected airway and vascular smooth muscle cells, but also in alveolar fibroblasts, peribronchial and adventitial fibroblasts as well as in a restricted number of Cthrc1pos cells indicating a primed pro-fibrotic status of the non-injured lung. In Tam-Bleo lungs, minimal contribution of these cells to the Cthrc1pos pool was observed. By contrast, labeling of Acta2pos cells following bleo administration (Bleo-Tam) led to massive labeling of Cthrc1pos cells, which following fine clustering were grouped into 4 subclusters named F1-F4. Interestingly, cells in cluster F1 were identified as Cthrc1low and displayed a strong LIF signature (LIFhigh) while cells in cluster F2 were LIFlow and Cthrc1high. Examination of F1 and F2 subclusters during fibrosis resolution suggested that F2 transition back to an F1 status and eventually differentiate into Cthrc1low LIFhigh alveolar fibroblasts. Analysis of the alveolar fibroblast cluster revealed the presence of three subclusters (A, B and C). Cluster C appeared only in Bleo-Tam and displayed a fibrotic signature (Sfrp1, Eln, Ltbp2, Spp1high). These cells, which originate from Acta2neg alveolar fibroblasts are suggested to differentiate into the Cthrc1low LIFhigh F1 subcluster. Data mining of human scRNA-seq from fibrotic lungs supported the conservation of the heterogeneity of the CTHRC1pos population. Alveolosphere assays indicated that resident mesenchymal cells did not reacquire their stem cell niche function at day 60, during fibrosis resolution. Answer to the question: Our results support a LIF-to-aMYF reversible switch during fibrosis formation and resolution.
2025-02-12 | GSE221402 | GEO
Project description:Question addressed in the study: Genetic lineage tracing of alpha smooth muscle actin-positive (ACTA2+) cells in the context of bleomycin-induced pulmonary fibrosis in mice has shown that activated myofibroblasts (aMYFs) differentiate into lipofibroblasts (LIFs) during fibrosis resolution. However, the heterogeneity of the different mesenchymal cell subclusters during fibrosis formation and their contribution to the aMYFs as well as the fate of aMYFs during fibrosis resolution are still unclear. Materials and methods: Two-month-old Tg(Acta2-CreERT2); tdTomatoflox mice were used to label Acta2pos cells before (Tam-Bleo condition) or after (Bleo-Tam condition) bleomycin administration. Using scRNA-seq, the origin and fate of Acta2pos cells converging on the aMYF/Cthrc1pos myofibroblast lineage, were analyzed at the peak of fibrosis formation (day 14) as well as during resolution (day 60). Mining of human IPF scRNA-seq data was also carried out. The function of resident mesenchymal cells derived from saline or bleomycin-injured lungs during fibrosis formation or resolution in supporting AT2 progenitor cell renewal was assessed using alveolar organoid assays. Results: By employing the dimensionality reduction and UMAP visualization MYF/Cthrc1pos cells were identified and characterized in three scRNA-seq conditions: Saline, Tam-Bleo and Bleo-Tam. Acta2pos cells isolated from saline-treated mice revealed the presence of Acta2pos cells in the expected airway and vascular smooth muscle cells, but also in alveolar fibroblasts, peribronchial and adventitial fibroblasts as well as in a restricted number of Cthrc1pos cells indicating a primed pro-fibrotic status of the non-injured lung. In Tam-Bleo lungs, minimal contribution of these cells to the Cthrc1pos pool was observed. By contrast, labeling of Acta2pos cells following bleo administration (Bleo-Tam) led to massive labeling of Cthrc1pos cells, which following fine clustering were grouped into 4 subclusters named F1-F4. Interestingly, cells in cluster F1 were identified as Cthrc1low and displayed a strong LIF signature (LIFhigh) while cells in cluster F2 were LIFlow and Cthrc1high. Examination of F1 and F2 subclusters during fibrosis resolution suggested that F2 transition back to an F1 status and eventually differentiate into Cthrc1low LIFhigh alveolar fibroblasts. Analysis of the alveolar fibroblast cluster revealed the presence of three subclusters (A, B and C). Cluster C appeared only in Bleo-Tam and displayed a fibrotic signature (Sfrp1, Eln, Ltbp2, Spp1high). These cells, which originate from Acta2neg alveolar fibroblasts are suggested to differentiate into the Cthrc1low LIFhigh F1 subcluster. Data mining of human scRNA-seq from fibrotic lungs supported the conservation of the heterogeneity of the CTHRC1pos population. Alveolosphere assays indicated that resident mesenchymal cells did not reacquire their stem cell niche function at day 60, during fibrosis resolution. Answer to the question: Our results support a LIF-to-aMYF reversible switch during fibrosis formation and resolution.
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Study Design: historical control
| 2671639 | ecrin-mdr-crc