MicroRNA expression data in mouse fetal lungs
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE41413 | GEO | 2013/11/26
SECONDARY ACCESSION(S): PRJNA176892
REPOSITORIES: GEO
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Project description:Microarray data of mouse postnatal lungs between day 1 and 6 weeks of age. The results provide a general insight into the microRNA expression profile during the alveolar phase of lung development. We obtained lung tissue of healthy postnatal mice, 4-5 replicates at each time point. Time points were day1, day4, day7, day14, and day 42.
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Project description:Microarray data of mouse postnatal lungs between day 1 and 6 weeks of age. The results provide a general insight into the gene expression profile during the alveolar phase of lung development.
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Project description:Microarray data of mouse postnatal lungs between day 1 and 6 weeks of age. The results provide a general insight into the gene expression profile during the alveolar phase of lung development. We obtained lung tissue of healthy postnatal mice, 4-5 replicates at each time point. Time points were day1, day4, day7, day14, and day 42.
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Project description:Microarray data of human fetal lungs between 16-23 weeks of gestation. The results provide a general insight into the microRNA expression profile during the canalicular phase of lung development.
2015-11-26 | GSE58139 | GEO
Project description:Microarray data of human fetal lungs between 16-23 weeks of gestation. The results provide a general insight into the microRNA expression profile during the canalicular phase of lung development. Lung tissue samples for microarray analysis were obtained through the University of Pittsburgh Health Sciences Tissue Bank through an approved IRB protocol and de-identified using an honest broker system. Total RNA was labeled with Cy3 and hybridized on Agilent 8X15K microRNA array (Agilent Technologies, Santa Clara, CA). After 20 hours hybridization, arrays were washed and scanned according to the manufacturerâs protocol.
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Project description:We hypothesize that gene expression in the lungs of these differentially-treated mice are divergent thus contributing to the disparity in their phenotypes. More specifically, (1) Effects of Leptin-treatment of ob/ob postnatal mice lungs are known to be volume-dependent from 2 to 10 wks of age, and are independent of the hypometabolism associated with leptin deficiency. ; (2) Leptin is critical to postnatal lung remodeling, particularly related to enlarged alveolar surface area. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between lungs of leptin or saline-treated ob/ob postnatal mice. Experiment Overall Design: This study utilizes microarray analysis to test these hypotheses. Three sets of lungs were harvested from both treatments (Leptin or Saline) at around 1 mo. postnatal. RNA was isolated and used for global gene expression profiling (Affymetrix Mouse 430A array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05.
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Project description:We hypothesize that gene expression in the lungs of these differentially-treated mice are divergent thus contributing to the disparity in their phenotypes. More specifically, (1) Effects of Leptin-treatment of ob/ob postnatal mice lungs are known to be volume-dependent from 2 to 10 wks of age, and are independent of the hypometabolism associated with leptin deficiency. ; (2) Leptin is critical to postnatal lung remodeling, particularly related to enlarged alveolar surface area. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between lungs of leptin or saline-treated ob/ob postnatal mice. Keywords: leptin, ob, lung
2008-06-01 | GSE10915 | GEO
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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
Project description:Pulmonary fibrosis is a disease characterized by inflammatory cell infiltration, scar formation, deposition of extracellular matrix, alveolar epithelial cell injury and hyperplasia. To determine if alterations in microRNA expression contribute to these phenotypes, microRNA expression profiling of the lungs from bleomycin treated C57Bl/6J mice, relative to that of untreated controls, was undertaken. Mice were treated at 8 weeks old with 100 Units/kg of bleomycin delivered subcutaneously with osmotic minipumps. At 42 days post treatment mice were euthanized and lung microRNA isolated. We identified 11 microRNA's to be significantly differentially expressed (FDR threshold of 0.01) in the lungs of bleomycin treated mice and confirmed these data with real time PCR measurements. These included bleomycin upregulated miR-34a, 335-5p, 207, 21, 301a, 146b, 199a-5p, and 449a and bleomycin downregulated miR-151-3p, 26a and 676. We have previously shown that 1558 genes are differentially expressed in the lungs of bleomycin treated mice. Of the 1412 targets of upregulated microRNAs, 142 were confirmed to be downregulated in the gene expression profile (GEP). Of the 583 targets of downregulated microRNAs, 53 were confirmed to be upregulated in the gene expression profile. Pathway analysis of the microRNA targets and GEP overlapping genes indicated that altered microRNA expression is associated with cellular development, cellular growth, cellular proliferation and changed tissue/cell morphology. Specific pathways include HGF signaling, Cholecystokinin/Gastrin-mediated signaling, Endothelin-1 signaling, RAR activation, Phospholipase C signaling and IGF1 signaling. We conclude that altered microRNA expression is a feature of pulmonary fibrosis which putatively influences components of the altered airway disease.
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