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Alveolar septation

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE479 | GEO | 2003/07/16

SECONDARY ACCESSION(S): PRJNA85163

REPOSITORIES: GEO

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Transcription profiling of lungs of wild type and Mg-delta strain of fibrillin-1deficient mice to identify pathways that are critical for normal alveolar septation

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

Fra-2 negatively regulates postnatal alveolar septation by modulating myofibroblast function

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

Alveoli septation inhibition and protection

Project description:It has been shown that dexamethasone (Dex) impairs the normal lung septation that occurs in the early postnatal period. Treatment with retinoic acid (ATRA) abrogates the effects of Dex. To understand the molecular basis for the Dex indiced inhibition of the formation of the alveoli and the ability of ATRA to prevent the inhibition of septation, gene expression was analyzed in 4-day old mice treated with diluent (control), Dex-treated and ATRA+Dex-treated. Keywords: other

2003-07-16 | GSE484 | GEO

Mus musculus

Project description:Alveolar septation

| PRJNA85163 | ENA

Regulation of alveolar septation by microRNA-489.

Project description:MicroRNAs (miRs) are small conserved RNA that regulate gene expression. Bioinformatic analysis of miRNA profiles during mouse lung development indicated a role for multiple miRNA, including miRNA-489. miR-489 increased on completion of alveolar septation [postnatal day 42 (P42)], associated with decreases in its conserved target genes insulin-like growth factor-1 (Igf1) and tenascin C (Tnc). We hypothesized that dysregulation of miR-489 and its target genes Igf1 and Tnc contribute to hyperoxia-induced abnormal lung development. C57BL/6 mice were exposed to normoxia (21%) or hyperoxia (85% O2) from P4 to P14, in combination with intranasal locked nucleic acid against miR-489 to inhibit miR-489, cytomegalovirus promoter (pCMV)-miR-489 to overexpress miR-489, or empty vector. Hyperoxia reduced miR-489 and increased Igf1 and Tnc. Locked nucleic acid against miR-489 improved lung development during hyperoxia and did not alter it during normoxia, whereas miR-489 overexpression inhibited lung development during normoxia. The 3' untranslated region in vitro reporter studies confirmed Igf1 and Tnc as targets of miR-489. While miR-489 was of epithelial origin and present in exosomes, its targets Igf1 and Tnc were produced by fibroblasts. Infants with bronchopulmonary dysplasia (BPD) had reduced lung miR-489 and increased Igf1 and Tnc compared with normal preterm or term infants. These results suggest increased miR-489 is an inhibitor of alveolar septation. During hyperoxia or BPD, reduced miR-489 and increased Igf1 and Tnc may be inadequate attempts at compensation. Further inhibition of miR-489 may permit alveolar septation to proceed. The use of specific miRNA antagonists or agonists may be a therapeutic strategy for inhibited alveolarization, such as in BPD.

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Transcription profiling of rat lung alveolar development

Project description:Lung alveolarization is a complex process that involves interactions between several cell types and leads to considerable increase in gas-exchange surface area. The step designated secondary septation includes elastogenesis from interstitial fibroblasts. We used microarrays to detail the global programme of fibroblast gene expression that underly secondary septation, and identified numerous genes that undergo signficant changes in expression Experiment Overall Design: Rat lung fibroblats were extemporaneously isolated at successive stages of postnatal development that flank the septation period for RNA extraction and hybridization on Affymetrix microarrays. Three biological replicates from three different litters were prepared for each time point.

2008-06-15 | E-GEOD-7491 | biostudies-arrayexpress

Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation

Project description:Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation

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Transcriptome analysis of a novel alveolar porcine epithelial cells line infected with different live attenuated Influenza Viruses

Project description:The project aim at studying transcriptional changes by BRB-seq of porcine alveolar epithelial cells line infected with wild type influenza virus compared to live attenuated influenza viruses. In addition, primary porcine nasal epithelial cells was also added to be able to compare how the alveolare epithelial cells line compare to primary cells. Finally, additional positive control including procine alveolar epithelial cells stimulated with Poly I:C or infected with IFN inducing Sendei virus was added.

2023-08-31 | E-MTAB-13128 | biostudies-arrayexpress

Expression data from rat lung alveolar development

2007-04-12 | GSE7491 | GEO

Fra-2 negatively regulates postnatal alveolar septation by modulating myofibroblast function.

Project description:Mice that globally overexpress the transcription factor Fos-related antigen-2 (Fra-2) develop extensive pulmonary fibrosis and pulmonary vascular remodeling. To determine if these phenotypes are a consequence of ectopic Fra-2 expression in vascular smooth muscle cells and myofibroblasts, we generated mice that overexpress Fra-2 specifically in these cell types (?-SMA-rtTA;tetO-Fra-2). Surprisingly, these mice did not develop vascular remodeling or pulmonary fibrosis but did develop a spontaneous emphysema-like phenotype characterized by alveolar enlargement. Secondary septa formation is an important step in the normal development of lung alveoli, and ?-smooth muscle actin (SMA)-expressing fibroblasts (myofibroblasts) play a crucial role in this process. The mutant mice showed reduced numbers of secondary septa at postnatal day 7 and enlarged alveolae starting at postnatal day 12, suggesting impairment of secondary septa formation. Lineage tracing using ?-SMA-rtTA mice crossed to a floxed TdTomato reporter revealed that embryonic expression of ?-SMA Cre marked a population of cells that gave rise to nearly all alveolar myofibroblasts. Comprehensive transcriptome analyses (RNA sequencing) demonstrated that the overwhelming majority of genes whose expression was significantly altered by overexpression of Fra-2 in myofibroblasts encoded secreted proteins, components of the extracellular matrix (ECM), and cell adhesion-associated genes, including coordinate upregulation of pairs of integrins and their principal ECM ligands. In addition, primary myofibroblasts isolated from the mutant mice showed reduced migration capacity. These findings suggest that Fra-2 overexpression might impair myofibroblast functions crucial for secondary septation, such as myofibroblast migration across alveoli, by perturbing interactions between integrins and locally produced components of the ECM.

| S-EPMC6842869 | biostudies-literature

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