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Transcriptome of type 2 alveolar epithelial cells (AT2 cells) with DNMT1 inihibition in vivo

ABSTRACT: Transcriptome of type 2 alveolar epithelial cells (AT2 cells) with DNMT1 inihibition in vivo

PROVIDER: PRJNA1160307 | ENA |

REPOSITORIES: ENA

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Transcriptome of type 2 alveolar epithelial cells (AT2 cells) with DNMT1 inihibition in vivo

Project description:DNA methylation patterns alter with age. However, it remains largely unknown how suppression of DNA methyltransferase changes the DNA methylation in AT2 cells. Here we looked into the transcriptome of AT2 with in vivo treatment of DNMT1 inhibitor in young mice and inverstigated how that alters the transcriptome.

2024-09-16 | GSE277061 | GEO

Evaluation of the impact of genetically suppression of DNA methyltransferase 1 (DNMT1) in aged vs young type 2 alveolar epithelial cells (AT2).

Project description:Using somatic genetic approaches, we aim for investigating the role of DNMT1 suppression in the regulation of transcriptom of young AT2 cells, in comparing with the effect of aging.

2024-09-25 | GSE277210 | GEO

The single cell RNA seq of pulmonary alveolar type II (AT2) cells

Project description:The pulmonary alveolar epithelium mainly composed of two types of epithelial cells: alveolar type I (AT1) and type II (AT2) cells. AT2 cells are the alveolar stem cells, and can differentiate into AT1 cells post-pneumonectomy (PNX). Here, we found that, compared with control mice (Sftpc-CreER; Cdc42flox/+; Rosa26-mTmG) at post-PNX day 21, Cdc42 AT2 null mice (Sftpc-CreER; Cdc42flox/-; Rosa26-mTmG) at post-PNX day 21 undergone fibrotic change. By using 10X genomics “Chromium Single Cell” technology, we performed single-cell RNA-seq analyses of AT2 cells of sham treated control mice (C0), AT2 cells of control mice at post PNX day 21 (C21) , AT2 cells of sham treated Cdc42 AT2 null mice (N0), and AT2 cells of Cdc42 AT2 null mice at post PNX day 21 (N21). The study identified a specific gene signature in AT2 cells of Cdc42 AT2 null mice at post PNX day 21 which is related to the fibrosis phenotype of Cdc42 AT2 null mice.

2020-01-03 | GSE138585 | GEO

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

Profiling AT1 and AT2 cells throughout alveolar development

Project description:This experiment profiled the transcriptomes of developing AT1 and AT2 cells from the beginning of embryonic alveolar development through the end of alveologenesis at 6 weeks of age.

2021-05-20 | GSE148487 | GEO

Profiling AT1 and AT2 cells throughout alveolar development

Project description:Profiling AT1 and AT2 cells throughout alveolar development

| PRJNA624469 | ENA

Evaluation of the impact of genetically suppression of DNA methyltransferase 1 (DNMT1) in aged vs young type 2 alveolar epithelial cells (AT2).

Project description:Evaluation of the impact of genetically suppression of DNA methyltransferase 1 (DNMT1) in aged vs young type 2 alveolar epithelial cells (AT2).

| PRJNA1161178 | ENA

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

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

| PRJNA835085 | ENA

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

Inflammatory Signals induce AT2 Cell-Derived Damage-Associated Transient Progenitors that Mediate Alveolar Regeneration

Project description:Tissue regeneration is a multi-step process mediated by diverse cellular hierarchies and states that are also implicated in tissue dysfunction and pathogenesis. Here, we leveraged single-cell RNA sequencing in combination with in vivo lineage tracing and organoid models to finely map the trajectories of alveolar lineage cells during injury repair and lung regeneration. We identified a distinct AT2-lineage population, Damage-Associated Transient Progenitors (DATPs), that arises during alveolar regeneration. We found that interstitial macrophage-derived IL-1β primes a subset of AT2 cells expressing Il1r1 for conversion into DATPs via a HIF1α-mediated glycolysis pathway, which is required for mature AT1 cell differentiation. Importantly, chronic inflammation mediated by IL-1β prevents AT1 differentiation, leading to aberrant accumulation of DATPs and impaired alveolar regeneration. Together, this step-wise mapping to cell fate transitions shows how an inflammatory niche impairs alveolar regeneration by controlling stem cell fate and behavior.

2020-08-03 | GSE144468 | GEO

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