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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Dan Wang

PROVIDER: E-GEOD-24465 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2011-09-29 | GSE24465 | GEO

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. 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.

2012-12-31 | E-GEOD-37080 | 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

Genomic landscape of the developing kidney upon conditional and time-dependent knockout of Wt1

Project description:We are characterizing global expression in the whole kidney at developmental stage E18.5, where we have used three Cre strains that result in knock out Wt1 in different cell types during renal development. Here the purpose is to identify the developmental stage at which the loss of Wt1 impacts kidney development, specifically in the context of a degree of disruption capable of ending in pediatric kidney cancers. Total RNA was isolated from whole kidneys of E18.5 mouse embryos following a variety of conditional knockouts of Wt1, plus appropriate control animals.

2015-07-27 | E-GEOD-70892 | 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

Hmga2 is required for canonical WNT signaling during lung development

Project description:The high-mobility-group (HMG) proteins are the most abundant non-histone chromatin-associated proteins. Here we deciphered the role of the high mobility group AT-hook protein 2 (HMGA2) during lung development by analyzing the lung of Hmga2 deficient mice (Hmga2-/-).We found that Hmga2 is expressed in the mouse embryonic lung at the distal airways. Analysis of Hmga2-/- mice showed that Hmga2 is required for proper cell proliferation and distal epithelium differentiation during embryonic lung development. Hmga2 knockout (KO) led to enhanced canonical WNT signaling due to an increased expression of secreted WNT glycoproteins Wnt2b, Wnt7b and Wnt11 as well as a reduction of the WNT signaling antagonizing proteins GATA6 (GATA binding protein 6) and FZD2 (frizzled homolog 2). Comparison of Hmga2-/- with Hmga2+/+ mice by Affymetrix microarray-based expression analysis of embryonic lung revealed an increased expression of genes whose products participate in cell cycle and canonical Wnt signaling. Affymetrix microarray transcriptome analysis of Hmga2-/- and Hmga2+/+ embryonic lung (E18.5) was performed and analyzed

2014-03-07 | E-GEOD-55340 | biostudies-arrayexpress

Transcription profiling by array of mouse Cdx2 knock out intestinal epithelium

Project description:RNAs were extracted from E18.5 control and Cdx2/villin-cre mutant ileums. We aim to identify the gene network changes in the mutant epithelia. We are especially interested in genes related with proliferation, apoptosis and cell differentiation.

2010-06-23 | E-MTAB-218 | biostudies-arrayexpress

Gene expression in the mouse embryonic small intestine in the presence or absence of E-cadherin

Project description:Gene expression was compared between E18.5 E-cadherin conditional knockout (cKO) small intestine and E18.5 control mouse small intestine. E18.5 mouse small intestine was collected from control and E-cadherin conditional knockout mice. RNA was prepared. Affymetrix Mouse Gene 1.0 gene arrays were used to interrogate gene expression. Data was analyzed using dChip software.

2012-02-28 | E-GEOD-31771 | biostudies-arrayexpress

Gene expression in the mouse embryonic small intestinal epithelium in the presence or absence of GATA4 and GATA6

Project description:Gene expression was compared between E18.5 Gata4Gata6 double conditional knockout (cKO) small intestinal epithelium and E18.5 control mouse small intestinal epithleium. E18.5 mouse small intestine was collected from control and Gata4Gata6 double conditional knockout mice. Epithelial cells were isolated, and RNA was prepared. Affymetrix Mouse Gene 1.0 gene arrays were used to interrogate gene expression. Data was analyzed using dChip software.

2014-04-30 | E-GEOD-49471 | biostudies-arrayexpress

The expression profiling comparison of mice with Scap and Insig deletion from perinatal lung (E17.5-PN1)

Project description:In this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung. Through comprehensive data analysis and integration, time dependent effects of epithelial SCAP/INSIG/SREBP deletion and defined SCAP/INSIG/SREBP-associated genes, bioprocesses and downstream pathways were identified. Total lung RNA was isolated from Scapdelata/delta, Insig1/2delta/delta, and respective control littermates at E17.5, E18.5 and PN1 were used for mRNA expression profiling analysis (n=3 for each condition)

2014-07-10 | E-GEOD-53397 | biostudies-arrayexpress

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