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RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen and 2 weeks of chase

ABSTRACT: We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment plus 2 weeks without tamoxifen. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the fluorescent reporter gene Katushka (located at an independent locus), by detecting Katushka fluorescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE115186 | GEO | 2018/06/25

REPOSITORIES: GEO

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RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen

Project description:We report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the reporter gene LacZ (located next to the oncogene in the same polycistronic mRNA), by loading CD31-/CD45- pneumocytes with the LacZ-activated fuorogenic molecule FDG prior to FACS sorting.

2018-06-25 | GSE115179 | GEO

RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen

Project description:RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen

| PRJNA474025 | ENA

RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen and 2 weeks of chase

Project description:RNAseq of CD31-/CD45- pneumocytes after 4 weeks of KRasG12V activation by tamoxifen and 2 weeks of chase

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Comparison of KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes

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Gene expression data from type II pneumocytes from adult mice with and without Trf2

Project description:Gas exchange in the mammalian lung occurs in the alveolar sacs lined by epithelial cells that form a barrier allowing effective oxygen diffusion. Telomere syndromes have their most common manifestation in degenerative disease of the alveoli, both pulmonary fibrosis and emphysema. We tested the role of telomere dysfunction by inducing deletion of the telomere binding protein Trf2 in type 2 alveolar epithelial cells (AEC2s) that both express the gene encoding surfactant protein C and constitute the regenerative compartment of the alveolar epithelium. Acquired telomere dysfunction in these cells preferentially induced cellular senescence, and mouse lungs were marked by an inflammatory response even though the telomere dysfunction was restricted to the epithelium. Senescent AECs had altered gene expression that differentially fell in inflammatory cell signaling pathways. Bleomycin challenge was uniformly fatal, and Trf2-depleted cells failed to generate clonal alveolar colonies in vitro. The telomere dysfunction response in AEC2s was in part p53-dependent, and we found evidence of a p53-mediated paracrine survival signal to the mesenchyme. These data indicate that telomere dysfunction in the alveolar epithelium limits its regenerative capacity and is sufficient to induce inflammation. It may thus be a primary driving event in telomere-mediated lung disease. Efforts to restore epithelial regenerative capacity may be an effective approach in a subset of fibrosis and emphysema patients. We studied the gene expression changes in adult type II pneumocytes 7 days after deleting Trf2. Mice carried floxed allele of Trf2 and mTmG reporter allele. Type II pneumocytes were collected by FACs sorting GFP+ cells from lungs 7 days after administering tamoxifen. 6 total samples were analysed. Three were from control samples that were heterozygous for Trf2 and three samples had Trf2 deleted.

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Effect of transcription inhibitor DRB on gene expression under KRASG12V induction of SAEC

Project description:To investigate RNA expression sensitive to DRB, we induced KRASG12V in SAEC cells with or without DRB treatment. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different conditions.

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Comparison of KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes

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Gene expression data from type II pneumocytes from adult mice with and without Trf2

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Transcriptomic analysis of murine lung tumor cells upon genetic KrasG12V ablation

Project description:To identify the mechanisms driving resistance upon KrasG12V ablation, we established lung cancer cell lines that carried loxP sequences flanking the exon 1 of Kras containing the G12V mutation (Kras +/loxG12Vlox), and lacked Trp53 alleles (Trp53 -/-). Tumor cells were infected with Adeno-Cre particles to excise the floxed sequences and individual cells that survived were expanded for further analysis.

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Comparison of Kras;Rank+/+ and Kras;Rankfl/fl mouse primary pneumocytes treated with Rankl ex vivo

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