Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Disruption of sorting nexin 5 causes respiratory failure associated with undifferentiated alveolar epithelial type I cells in mice

ABSTRACT: Deletion of Snx5 leads to respiratory failure in neonatal mice. Here we analyzed the effect of depleted SNX5 in a lung. We used expression microarray to compare between wild lungs and mutant lungs at E18.5 and E18.5 after air-breathing test. Total RNA were extracted from embryonic 18.5 day (E18.5) wild and mutant mice lung. Also other total RNA samples were extracted after air-breathing test at E18.5.

ORGANISM(S): Mus musculus

SUBMITTER: Hyobean Jeong

PROVIDER: E-GEOD-37080 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Disruption of sorting nexin 5 causes respiratory failure associated with undifferentiated alveolar epithelial type I cells in mice

Project description:Deletion of Snx5 leads to respiratory failure in neonatal mice. Here we analyzed the effect of depleted SNX5 in a lung. We used expression microarray to compare between wild lungs and mutant lungs at E18.5 and E18.5 after air-breathing test.

2012-12-31 | GSE37080 | GEO

Mouse embryonic lung FOXF1 ChIP-seq analysis

Project description:FOXF1 targets in embryonic day 18.5 mouse lungs were determined using FOXF1 immunoprecipitation followed by sequencing. FOXF1 binding sites in two biological replicates of pooled E18.5 wildtype mouse lungs (n=3) were to a 2% input control sample.

2016-09-01 | E-GEOD-77951 | biostudies-arrayexpress

Microarray of Mst1/2 deleted epithelial cells from E18.5 mouse lungs

Project description:ShhCre;Mst1/2flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from epithelial progenitors during lung morphogenesis. Lungs from E18.5 control and Mst1/2 D/D mice were mechanically and enzymatically dissociated to generate single cell suspension. Epcam(+) cells were isolated using magnetic microbeads. Microarray analysis of mRNAs isolated from Epcam(+) epithelial cells from E18.5 control and Mst1/2 D/D mice was performed to identify transcriptional changes following deletion of the mammalian Hippo kinases (Mst1 and Mst2) from the embryonic lung. The mammalian Hippo kinases, Mst1 and Mst2, were conditionally deleted in epithelial progenitors of the developing lung using ShhCre. Epcam(+) epithelial cells were isolated from the lungs of E18.5 control and Mst1/2 deleted mice. mRNA isolated from Epcam(+) epithelial cells was analyzed by microarray.

2015-01-01 | E-GEOD-61582 | biostudies-arrayexpress

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

Project description:Insight into the role of Insulin-like Growth Factor (IGF) in development of lungs has come from the study of genetically modified mice. IGF1 is a key factor during lung development. IGF1 deficiency in the neonatal mouse causes respiratory failure collapsed alveoli and altered alveolar septa. To further characterize IGF1 function during lung development we analyzed Igf1-/- mouse prenatal lungs in a C57Bl/6 genetic background. Mutant lungs showed disproportional hypoplasia, disorganized extracellular matrix and dilated alveolar capillaries. IGF1 target genes during lung maturation were identified by analyzing RNA differential expression in Igf1-/- lungs using microarrays. Lungs from E18.5 were isolated from both Igf1+/+ wild type and Igf1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos at embrionic (E) stage 18.5 days post coitum (E18.5). 3 biological replicates per genotype.

2014-03-31 | E-GEOD-17157 | biostudies-arrayexpress

Mesenchymal Nuclear factor I B regulates cell proliferation and epithelial differentiation during lung maturation

Project description:We generated Nfibf/f mice and then cross with Dermo1-Cre mice to obtain Nfibf/f, Dermo1-Cre mice. In these Nfibf/f, Dermo1-Cre mice, there are defects in sacculation and epithelial cell differentiation. We performed micoarray analysis to find the genes which are possibley regulated by NFI-B and related to lung maturation during lung development. We used microarrays to performing transcriptional profiling of Nfibf/f, Dermo1-Cre and Nfibf/f lungs at E18.5

2011-09-28 | E-GEOD-24465 | biostudies-arrayexpress

Smad1 and its target gene Wif1 coordinate BMP and Wnt signaling activities to regulate lung development

Project description:Bone morphogenetic protein 4 (BMP4) is essential for lung development. To define its intracellular signaling mechanisms by which BMP4 regulates lung development, BMP-specific Smad1 or Smad5 was selectively knocked out in fetal mouse lung epithelial cells. Abrogation of lung epithelial-specific Smad1, but not Smad5, resulted in retardation of lung branching morphogenesis and reduced sacculation, accompanied by altered distal lung epithelial cell proliferation and differentiation, and consequently severe neonatal respiratory failure. By combining cDNA microarray with ChIP-chip analyses, Wnt inhibitory factor-1 (Wif1) was identified as a novel target gene of Smad1 in the developing mouse lung epithelial cells. Loss of Smad1 transcriptional activation of Wif1 expression was associated with reduced Wif1 expression and increased Wnt/beta-catenin signaling activity in lung epithelia, resulting in specific fetal lung abnormalities. Therefore, a novel regulatory loop of BMP4-Smad1-Wif1-Wnt/beta-catenin in coordinating BMP and Wnt pathways to control fetal lung development is suggested. mRNA profiling: Total RNA was isolated from left lobe lungs of three pair of E18.5 wild type and Smad1 lung epithelium-specific conditional knockout mice

2011-01-07 | E-GEOD-26502 | biostudies-arrayexpress

Cole Lab Fred- genotypeRA experiment

Project description:Mammalian lung development during the saccular and alveolar stages is dependent upon antagonistic molecular signalling by endogenous retinoic acid (RA) and glucocorticoids (GCs) which regulate gene expression via the retinoic acid receptor (RAR) family and the glucocorticoid receptor (GR), respectively. The genomic mechanism of this antagonism was investigated with in vitro distal lung explant cultures from E18.5 GR-null (GR-/-) mice treated with all-trans-RA (atRA) for 2h . Whole mouse genome microarray analysis from lung explant tissue identified a small number of gene targets which were not only significantly induced by atRA in the wildtype lung, but also significantly stimulated to levels greater than atRA-treated wildtype lungs in GR-/- lungs.

2014-01-12 | E-MEXP-3833 | biostudies-arrayexpress

Quantitative proteomics analysis of lung tissue from E18.5 embryos with mesenchymal deletion of VLK

Project description:Vertebrate lonesome kinase (VLK) is the only known secreted tyrosine kinase and responsible for the phosphorylation of a broad range of secretory pathway-resident and extracellular matrix proteins. However, its cell-type specific functions in vivo are still largely unknown. Therefore, we generated mice with a mesenchyme-specific knockout of the VLK gene (protein kinase domain containing, cytoplasmic (Pkdcc)). Most of the homozygous mice die shortly after birth, most likely as a consequence of their lung abnormalities and consequent respiratory failure. E18.5 embryonic lungs showed a reduction of alveolar type II cells, smaller bronchi, and an increased lung tissue density. Global mass spectrometry-based quantitative proteomics identified 112 proteins with significantly and at least 1.5fold differential abundance between genotypes. Twenty-five of these had been assigned to the extracellular region and 15 to the mouse matrisome. Specifically, fibromodulin and matrilin 4, which are involved in extracellular matrix organization, were significantly more abundant in lungs from Pkdcc knockout embryos. These results support a role for mesenchyme-derived VLK in lung development through regulation of matrix dynamics and the resulting non-cell-autonomous modulation of alveolar epithelial cell differentiation.

2023-04-11 | PXD037700 | Pride

Transcription profiling of mouse Igf1 null mutant

Project description:Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons. We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes. Experiment Overall Design: Cochleae from two E18.5 were isolated from both Igf-1+/+ wild type and Igf-1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos 18.5 days post coitus (E18.5). Three independent pools were used. Cochlear tissues included the otic capsule but not vestibular tissues.

2008-10-21 | E-GEOD-11844 | biostudies-arrayexpress

Transcription profiling of mouse Igf-1 -/- and Igf-1+/+ cochleas

2009-02-10 | E-GEOD-11821 | biostudies-arrayexpress