Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA307182 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls. Primary tumor induced gene expression in AT-II cells from Tlr3-/- and WT mice was measured at 2 weeks after tumor inoculation subcutaneously. AT-II cells from mice without tumor bearing were set as controls.
2016-08-10 | E-GEOD-76397 | biostudies-arrayexpress
Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls.
2016-08-10 | GSE76397 | GEO
Project description:Background: LKB1 is among the most frequently altered tumor suppressors in lung adenocarcinoma. Inactivation of Lkb1 accelerates the growth and progression of oncogenic KRAS-driven lung tumors in mouse models. However, the molecular mechanisms by which LKB1 constrains lung tumorigenesis and whether the aggressive cancer state that stems from Lkb1 deficiency can be reverted remains unknown. By bulk gene expression profiling, Lkb1 restoration promotes the expression of markers and functions of alveolar type II cells, suggesting that LKB1 may govern a cell-state transition within the neoplastic epithelial compartment. Purpose: To determine whether the restoration of Lkb1 drives changes in cell state and/or abundance within established oncogenic KRAS-driven lung tumors. Approach: To control LKB1 function in vivo, we generated an Lkb1XTR allele, which enables Cre-mediated disruption of Lkb1 expression during tumor development and subsequent FLPo-ERT2-mediated reactivation of Lkb1 within established tumors. Lung tumors were initiated in KT;Lkb1XTR/XTR (non-restorable) and KT;Lkb1XTR/XTR;FLPo-ERT2 (restorable) mice with Lenti-Cre. Following tumor development, lung tumor-bearing were treated with either corn oil vehicle or tamoxifen for two weeks prior to isolating specifically neoplastic cells by FACS for single cell RNA-seq. Results: Single cell analysis revealed that the neoplastic epithelial compartment was composed of alveolar type I- and type II-like subpopulations, a Krt8+ transitional state, an actively proliferating subpopulations, and an indeterminate subpopulation partially resembling the alveolar type II-like identity. Dynamic inference analyses indicated that the indeterminate population represents an intermediate state along the alveolar type II to alveolar type I trans-differentiation trajectory. Notably, the indeterminate cluster was more proliferative than the alveolar type II-like subpopulation and exhibited higher expression of Sox9, which is a marker of distal lung epithelial progenitors. There was a marked shift in the epithelial compartment from the indeterminate state to alveolar type II epithelial-like identity in response to Lkb1 restoration. Conclusions: LKB1 governs the transition between a proliferative progenitor-like population and mature alveolar type II-like identity within oncogenic KRAS-driven lung tumors
2021-12-23 | GSE179502 | GEO
Project description:Background: LKB1 is among the most frequently altered tumor suppressors in lung adenocarcinoma. Inactivation of Lkb1 accelerates the growth and progression of oncogenic KRAS-driven lung tumors in mouse models. However, the molecular mechanisms by which LKB1 constrains lung tumorigenesis and whether the aggressive cancer state that stems from Lkb1 deficiency can be reverted remains unknown.Purpose: To assess the acute transcriptional response to Lkb1 restoration within established lung tumors in a genetically engineered mouse model of oncogenic KRAS-driven lung adenocarcinoma. Approach: To control LKB1 function in vivo, we generated an Lkb1XTR allele, which enables Cre-mediated disruption of Lkb1 expression during tumor development and subsequent FLPo-ERT2-mediated reactivation of Lkb1 within established tumors. Lung tumors were initiated in KrasLSL-G12D/+;R26LSL-tdTomato (KT; Lkb1 wild-type), KT;Lkb1XTR/XTR (non-restorable), and KT;Lkb1XTR/XTR;FLPo-ERT2 (restorable) mice with Lenti-Cre. Prior isolating neoplastic cells by FACS for gene expression profiling by RNA-seq, lung tumor-bearing were treated with either corn oil vehicle or tamoxifen for two weeks following tumor development. Results: Lkb1 restoration resulted in higher expression of markers of alveolar type II epithelial cells as well as gene sets relating to immunomodulation and lipid metabolism export, which are important functions of mature alveolar type II epithelial cells. Conclusions: LKB1 promotes the expression of C/EBP target genes and consequently drives features of alveolar type II epithelial cell differentiation.
2021-12-23 | GSE179500 | GEO
Project description:The amount of pulmonary surfactant within type II cells and in the alveolar space, referred to as surfactant pool sizes, are tightly regulated. The molecular pathways that sense and regulate surfactant pool size within the alveolus have not been identified and constitute a fundamental knowledge gap in the field. Our data show that mice with a germline mutation in the orphan G-protein-coupled receptor, GPR116, have a 30-fold accumulation of surfactant phospholipids that causes respiratory distress in adult animals. This phenotype is associated with increased surfactant secretion and induction of the purinergic receptor P2RY2 in young animals, and lipid-laden macrophages and alveolar destruction in older animals. We further demonstrate that GPR116 mRNA expression is developmentally regulated in the murine lung with peak expression at birth when surfactant pool sizes are maximal. Within the lung, GPR116 protein expression is restricted to the apical plasma membrane of alveolar type I and type II epithelial cells. To better understand the roles and molecular mechanisms by which Gpr116 influences gene expression in lung, the effect of cell-selective deletion of Gpr116 (Gpr116D/D) on genome-wide mRNA expression profiles was determined in murine type II alveolar epithelial cells. Differentially expressed genes were identified from Affymetrix Murine GeneChips analysis and subjected to gene ontology classification promoter analysis, pathway mapping and literature mining.
2013-04-10 | E-GEOD-41417 | biostudies-arrayexpress
Project description:We established a new protocol for negative immunomagnetic isolation of murine primary Type II alveolar epithelial cells (AEC II) yielding untouched primary murine AEC II. AEC II were collected from mice 24h after Aspergillus fumigatus or mock infection (9 replicates per experimental group) and analyzed by label-free quantitative proteomics.
2017-10-05 | PXD005834 | Pride
Project description:RNAseq of primary murine alveolar epithelial cells type II (AECII) and the murine lung cells MLE-15 in order to identify potential candidates of trypsin-like proteases capable to cleave the influenza surface glycoprotein hemaglutinine (HA). AECII cells do support the cleavage of HA while MLE-15 cells do not. In addition, leukocytes where sequenced as well.
2020-03-27 | E-MTAB-8571 | biostudies-arrayexpress
Project description:Previously, we identifed alveolar Type II cells as cell-of-origin for Kras induced lung adenocarcinoma. In the current study, we examined the phenotype of Type II cells after Kras activation and found evidence for proliferation of cells that co-express Type I and Type II markers. Using RNAseq, we are trying to charcterize these different alveolar epithelial cells (Type I, Type II and double positive (Type I/II+)) upon KrasG12D activation during lung adenocarcinoma.
2023-05-09 | GSE230664 | GEO
Project description:Expression data from alveolar type II epithelial cells
| PRJNA95401 | ENA
Project description:Analysis of human alveolar epithelial cell signatures at gene expression level. The aim of the study was to identify candidate genes that are induced in human alveolar epithelial type II cells on collagen-coated dishes. Results provide important information about changes hAT2 cells undergo in the transformation to AT1-like cells. Total RNA obtained from human alveolar epithelial cells grown on collagen- or matrigel-coated dishes for 12, 24, 48 and 72 hr.
2014-02-01 | E-GEOD-40516 | biostudies-arrayexpress