Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA374658 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5252820.fastq.gz | Fastqsanger.gz | |||
| SRR5252821.fastq.gz | Fastqsanger.gz | |||
| SRR5252822.fastq.gz | Fastqsanger.gz | |||
| SRR5252823.fastq.gz | Fastqsanger.gz | |||
| SRR5252824.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Purpose: Compare the transciptome between lung myofibroblasts that contituatively express Fra-2 to control lung myofibroblasts to determine genes that may contribute to regulation of secondary alveolar septation Methods: mRNa sequences from lung myofibroblasts isolated from mutant mice that contituatively express Fra-2 in α-SMA expressing cells (sma-Fra2) were compared to control mice. n=4 in each group Results: 43,432 transcripts wre analyzed and 361 genes were differentially expressed in the smaFra2 mice compared to wild type control. Functional analysis was performed using the Database for Annotation, Visualization and Integrated Discovery. Changes in genes from lung myofibroblasts in smaFra2 mice: genes involved with extracellular matrix and cell adhesion were upregulated; Ectonucleotide pyrophosphatase/phosphodiesterase family member 2 (Enpp2) and LPA receptor1 (LPA1) were downregulated. Coclusion: The secondary alveolar septation defect in smaFra2 mice could be explaned by Fra-2 mediated changes in extracellular matrix and cell adhesion in developing lung myofibroblasts.
2018-01-01 | GSE94857 | GEO
Project description:The Mg-delta strain of fibrillin-1 deficient mice display an early defect in alveolar septation. This study attempts to identify expression patterns in the mutant mouse lung compared to their wild-type littermates that suggest pathways that are critical for normal septation. This experiment focuses on postnatal days 1 and 5. Other time points will be added at a later date.
2007-11-06 | E-GEOD-479 | biostudies-arrayexpress
Project description:The Mg-delta strain of fibrillin-1 deficient mice display an early defect in alveolar septation. This study attempts to identify expression patterns in the mutant mouse lung compared to their wild-type littermates that suggest pathways that are critical for normal septation. This experiment focuses on postnatal days 1 and 5. Other time points will be added at a later date. Keywords: other
2003-07-16 | GSE479 | GEO
Project description:Alveolar myofibroblasts emerge during postnatal lung development and are substantially cleared following the completion of the alveolar stage of lung development. In this study, we hypothesized that alveolar myofibroblast descendants that escape apoptotic clearance are reactivated in resposne to injury during adult life.
2024-12-31 | GSE248726 | GEO
Project description:Postnatal respiration requires the bulk formation of alveoli that produces extensive surface area for gas diffusion from epithelium to the circulatory system. Alveolar morphogenesis initiates at late gestation or postnatal stage during mammalian development and is mediated by coordination among epithelial, mesenchymal and endothelial cells. Here we show that stromal cells produce Heparan Sulfate Glycosaminoglycan (HS-GAG) to maintain a niche for alveolar development by modulating both the biophysical and biochemical cues. HS is predominantly enriched in myofibroblasts in postnatal murine lungs, and genetic ablation of HS synthase gene Ext1 in fibroblast populations results in enlarged and simplified alveolar structures. HS is selectively required for the cell identity of a subset of alveolar myofibroblasts (PDGFRαhi αSMA+) residing in the distal alveolar region, which exhibit contractile properties and maintain WNT signaling activity to support normal proliferation and differentiation of alveolar epithelial cells. HS is essential to prevent precocious apoptosis of alveolar myofibroblasts. We show that these processes are dependent upon FGF/MAPK signaling and forced activation of MAPK/ERK signaling partially corrected alveolar simplification along with restoration of alveolar myofibroblast identity and AT2 cell proliferation in HS deficient mice. These data reveal HS as an essential orchestrator for developing alveolar niche critical for generation of gas exchange units.
2025-02-05 | GSE264370 | GEO
Project description:Postnatal respiration requires the bulk formation of alveoli that produces extensive surface area for gas diffusion from epithelium to the circulatory system. Alveolar morphogenesis initiates at late gestation or postnatal stage during mammalian development and is mediated by coordination among epithelial, mesenchymal and endothelial cells. Here we show that stromal cells produce Heparan Sulfate Glycosaminoglycan (HS-GAG) to maintain a niche for alveolar development by modulating both the biophysical and biochemical cues. HS is predominantly enriched in myofibroblasts in postnatal murine lungs, and genetic ablation of HS synthase gene Ext1 in fibroblast populations results in enlarged and simplified alveolar structures. HS is selectively required for the cell identity of a subset of alveolar myofibroblasts (PDGFRαhi αSMA+) residing in the distal alveolar region, which exhibit contractile properties and maintain WNT signaling activity to support normal proliferation and differentiation of alveolar epithelial cells. HS is essential to prevent precocious apoptosis of alveolar myofibroblasts. We show that these processes are dependent upon FGF/MAPK signaling and forced activation of MAPK/ERK signaling partially corrected alveolar simplification along with restoration of alveolar myofibroblast identity and AT2 cell proliferation in HS deficient mice. These data reveal HS as an essential orchestrator for developing alveolar niche critical for generation of gas exchange units.
2025-02-05 | GSE264371 | GEO
Project description:Palmitoylation negatively regulates AEG-1 function
| PRJNA888790 | ENA
Project description:Regulation of lung responses to air breathing and continued alveolar development shape ex-utero and adult respiratory health. Applying single-cell transposome hypersensitive site sequencing (scTHS-seq) to human and mouse lung, we assembled a regulatory atlas of postnatal lung development and analyzed over 80,000 single-cells. From day of life 1, we characterized cell types and cell-cell interactions driving alveoli generation. We elucidated key transcription factor-gene accessibility modules (TF-GAM) guiding alveolar epithelial cell differentiation and epithelial-mesenchymal interactions involved in alveolar septation and mechanotransduction. Incorporating GWAS causal variants, we identified lung pathogenic risk units enriched in specific cell types. Our regulatory map and analysis model provide an effective resource to investigate age-dependent and species-specific control of critical developmental processes. Furthermore, this resource complements single-cell atlas efforts to advance our understanding of lung health and disease across the human lifespan.
2020-12-31 | GSE154027 | GEO
Project description:The septation initiation network (SIN), composed of a conserved SepH (Cdc7p) kinase cascade, plays an essential role in fungal cytokinesis/septation and conidiation for asexual reproduction, while the mitogen-activated protein kinase (MAPK) pathway depends on successive signaling cascade phosphorylation to sense and respond to stress and environmental factors. In this study, a SepH suppressor–PomA in the filamentous fungus A. nidulans was identified as a negative regulator of septation and conidiation such that the pomA mutant was able to cure defects of sepH in septation and conidiation and overexpression of pomA remarkably suppressed septation. Under the normal cultural condition, SepH positively regulates the phosphorylation of MAPK-HogA, while PomA reversely affects this process and the phosphorylated HogA in MAPK could be a downstream product of the activated SIN. However, under the osmostress condition, the induced phosphorylated HogA is capable of bypassing the requirement of SepH to fulfill septation and conidiation. Findings demonstrate that crosstalk exists between the SIN and MAPK pathways.
2019-06-17 | PXD012514 | Pride