Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next generation sequencing facilitates quantitative analysis of transcriptomes of adult mouse alveolar epithelial type 2 (AT2) cells with Atf3 or Thra overexpression

ABSTRACT: Purpose: The goals of this study are to generate transcriptome profiling (RNA-seq) of AT2 cells with over expression of Atf3 and Thra. Methods: AT2 cell mRNA profiles of 5 or 6-week-old wild-type mice were generated by deep sequencing, in triplicate. The Illumina Nextseq 500 system was used to generate raw data at 75 cycles. Fastq files was aligned to the reference genome and DEseq2 was used to analyze the differentially expressed genes. Results: Our results show that Atf3 or Thra overexpression promotes the expression of genes associated AT2 cell proliferation. Conclusions: Our study represents the first detailed analysis of transcriptomes of mouse AT2 cell with Atf3 or Thra overexpression, with biologic replicates, generated by RNA-seq technology.

ORGANISM(S): Mus musculus

PROVIDER: GSE183129 | GEO | 2022/07/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ATF3 links host adaptive-response to breast cancer metastasis

Project description:Cancer-host interactions play an important role in cancer development. We identified ATF3, an adaptive-response gene, in the host to facilitate metastasis. We also demonstrated that the macrophage is one of the key cell types for host-ATF3 to function. Furthermore, matrix metalloproteases 9 is a functionally important target gene of ATF3 in co-culture assays. Gene profiling with bioinformatics analyses indicated that ATF3 downstream gene-signatures derived from tumor-associated macrophages in a mouse model can distinguish human tumor stroma from M-bM-^@M-^\distantM-bM-^@M-^] stroma in and can stratify the patients into high- versus low-risk groups. Importantly, multivariate analyses indicated that high expression of ATF3 itself in mononuclear cells within breast tumors is an independent predictor for breast cancer-specific death in a cohort of patients. Approximately 21 days after orthotopic injection of PyMT breast cancer cells into syngeneic C57BL/6 mice (WT or ATF3 KO hosts) tumors were removed (tumors were ~1 cm cubic in volume), enzymatically digested to generate single cell suspensions, stained, and sorted for F4/80 and CD45 double positive cells by FACS. Isolated cells were lysed in TRIzol, processed to generate total RNA, and gene expression analyzed by microarray. Four replicate WT TAM samples and four replicate ATF3 KO TAM samples were analyzed.

2013-07-10 | E-GEOD-36904 | biostudies-arrayexpress

DNA microarray studies of tumors grown in nude mice from breast cancer cells MDA-MB-231 overexpressing or not the angiotensin II AT2 receptor, and treated or not with AT2 agonist compound C21

Project description:This experiment aims at investigating the effect of AT2 overexpression and/or activation in breast cancer. Human breast cancer cells MDA-MB-231 were transfected with lentiviral construct containing flagged human AT2 receptor sequence (or empty vector) and were subcutaneously injected into immuno-deficient mice (2. 10e6 cells). When the tumors reached 5 mm3 volume, mice were treated daily with compound C21 (0.3 mg/kg) or vehicle for 43 days. Total RNA was extracted from tumors and submitted to DNA array analysis.

2020-11-07 | E-MTAB-8532 | biostudies-arrayexpress

Single cell sequencing facilitates quantitative analysis of transcriptomes of proliferative alveolar epithelial type 2 (AT2) cells in adult mouse lungs

Project description:Purpose: The goals of this study are to generate transcriptome profiling at single cell level (scRNA-seq) of proliferative AT2 cells Methods: Lungs of 6- to 10-week-old SPC-EGFP, Ki67-creRT2, Rosa26-tdTomato mice before and 4 days after Streptococcus pneumoniae infection-induced lung injury were dissociated using dispase digesting method. Proliferative AT2 cells (GFP+/tdTomato+) and non-proliferative AT2 cells (GFP+/tdTomato-) were sorted using a BD influx LSRII. AT2 cell mRNA profiles were generated by scRNA-seq. Sequencing was performed on an Illumina Nextseq 500 system operated by the Next Generation Sequencing at GENEWIZ using the HiSeq 2x150 bp high output sequencing kit. The scRNAseq data was processed by Cell Ranger (v.3.0.2, 10X Genomics) followed by Seurat suite (version 4.0.1). Results: Our results show a distinctive transcriptome profile of proliferative AT2 cells in adult mouse lungs Conclusions: Our study represents the first detailed analysis of transcriptomes of proliferative and non-proliferative AT2 cells in adult mouse lungs generated by scRNA-seq technology.

2022-07-21 | GSE184405 | GEO

AT2 COPD Transcriptomics

Project description:We generated transcriptomes of primary human lung AT2 cells isolated from distal parenchyma of ex-smoker controls and COPD patients, with both mild and severe disease.

| EGAS00001007387 | EGA

Gene expression profile at single cell level of total alveolar type II (AT2) cells and CD44hi AT2 cells

Project description:AT2 cells are the resident progenitor cells in alveoli, capable of self-proliferation and differentiation into alveolar type I cells during homeostatic maintenance and tissue regeneration. The AT2 cell population is heterogenous. We identified a small subpopulation of AT2 cells that express high levels of CD44 (CD44hi) and display progenitor functions during alveoli homeostasis. To further analyze the heterogeneity of the AT2 cell population and characterize CD44hi AT2 cells, we performed single cell RNA-seq on the total AT2 cell population and CD44hi AT2 cells.

2024-05-24 | GSE202226 | GEO

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

Gene expression of alveolar macrophage in mice with AT2 cell-specific Cpt1a deletion

Project description:Carnitine palmitoyltransferase 1a (CPT1a) is the key regulator of mitochondrial long-chain fatty acid beta-oxidation (LCFAO). However, the functional significance of AT2 cell-specific LCFAO at baseline and during acute lung injury (ALI) is not fully understood. In this study, Murine models of AT2 cell-specific Cpt1a deletion were generated for investigating the role of CPT1a in regulating AT2 cell function and the severity of lipopolysaccharide-induced murine ALI models.

2024-07-05 | GSE255949 | GEO

Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4+ endothelial cells

Project description:Exercise is a powerful driver of physiological angiogenesis during adulthood, but the mechanisms of exercise-induced vascular expansion are poorly understood. We explored endothelial heterogeneity in skeletal muscle and identified two capillary muscle endothelial cells (mEC) populations which are characterized by differential expression of ATF3/4. Spatial mapping showed that ATF3/4 + mECs are enriched in red oxidative muscle areas while ATF3/4 low ECs lie adjacent to white glycolytic fibers. In vitro and in vivo experiments revealed that red ATF3/4 + mECs are more angiogenic when compared to white ATF3/4 low mECs. Mechanistically, ATF3/4 in mECs control genes involved in amino acid uptake and metabolism and metabolically prime red (ATF3/4 + ) mECs for angiogenesis. As a consequence, supplementation of non-essential amino acids and overexpression of ATF4 increased proliferation of white mECs. Finally, deleting Atf4 in ECs impaired exercise-induced angiogenesis. Our findings illustrate that spatial metabolic angiodiversity determines the angiogenic potential of muscle ECs.

2021-06-15 | GSE174785 | GEO

AT2 COPD Methylomics

Project description:We generated genome-wide DNA methylation maps at single CpG resolution of primary human lung AT2 cells isolated from distal parenchyma of ex-smoker controls and COPD patients, with both mild and severe disease

| EGAS00001007386 | EGA

Etv5 ChIP-seq in AT2 cells

Project description:Alveolar type II (AT2) cell dysfunction contributes to a number of significant human pathologies including respiratory distress syndrome, lung adenocarcinoma, and debilitating fibrotic diseases, but the critical transcription factors that maintain AT2 cell identity are unknown. Here we show that the E26 transformation-specific (ETS) family transcription factor Etv5 is essential tomaintain AT2 cell identity. Deletion of Etv5 from AT2 cells produced gene and protein signatures characteristic of differentiated alveolar type I (AT1) cells. Consistent with a defect in the AT2 stem cell population, Etv5 deficiency markedly reduced recovery following bleomycin-induced lung injury. Lung tumorigenesis driven by mutant KrasG12D was also compromised by Etv5 deficiency. ERK activation downstream of Ras was found to stabilize Etv5 through inactivation of the cullin- RING ubiquitin ligase CRL4COP1/DET1 that targets Etv5 for proteasomal degradation. These findings identify Etv5 as a critical output of Ras signaling in AT2 cells, contributing to both lung homeostasis and tumor initiation.

2018-03-08 | GSE111569 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data