Characterize the unique transcriptional changes in the embryonic trachea of knockout mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE27305 | GEO | 2014/02/14
SECONDARY ACCESSION(S): PRJNA137125
REPOSITORIES: GEO
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Project description:To further identify the transcriptional changes underlying congenital tracheal malformation in a1H knockout mice, the differential gene expression panel was examined by Affymetrix microarray. To investigate the roles of a1H-regulated genes in tracheal development, we characterize the unique transcriptional changes of early trachea in kockout mice, and compare the expression profiles of knock out trachea with those of wild type trachea. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up or down-regulated genes during this process. Mouse embryos trachea were collected at embryo day 16 (E16) for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homozygous mouse embryos trachea in order to compare with gene expression profile of wild type mouse tracheal.
2014-02-14 | E-GEOD-27305 | biostudies-arrayexpress
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Project description:The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 ± 15 pack-yr). Gene expression differences [fold-change >1.5, p< 0.01, Benjamini-Hochberg correction] were assessed with Affymetrix microarrays. 1,057 probe sets were differentially expressed in healthy smokers vs nonsmokers, representing >500 genes. Trachea gene expression was compared to an independent group of small airway epithelial samples (n=23 healthy nonsmokers, n=19 healthy smokers, 25 ± 12 pack-yr). The trachea epithelium is more sensitive to smoking, responding with 3-fold more differentially-expressed genes than small airway epithelium. The trachea transcriptome paralleled the small airway epithelium, with 156 of 167 (93%) genes that are significantly up- and down-regulated by smoking in the small airway epithelium showing similar direction and magnitude of response to smoking in the trachea. Trachea epithelium can be obtained without conscious sedation, representing a less invasive surrogate “canary” for smoking-induced changes in the small airway epithelium. This should prove useful in epidemiologic studies correlating gene expression with clinical outcome in assessing smoking-induced lung disease. Experiment Overall Design: Tracheal gene expression: matched group of small airway epithelial samples (n=23 healthy non-smokers, n= 19 healthy smokers)
2009-09-04 | E-GEOD-13933 | biostudies-arrayexpress
Project description:Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, which causes airway surface liquid and mucus dehydration, resulting in reduced mucus clearance and airway mucus obstruction. The data provided here represents mRNA expression data from dissected whole trachea (distal and proximal ends were cut 3-4 cartilage rings below the larynx and just above the bifurcation, respectively) from male WT and Scnn1b-Tg littermates (C57Bl/6N Tac background) at 4 time points [postnatal days (PND) 0, 3, 10, and 42]. Histologically, PND 0 trachea are normal, a tracheal mucus plug/obstruction develops around PND 3 and typically recedes to the intrapulmonary airways after PND 10, and the trachea is again histologically normal by PND 42. The data from the WT mice provides a global look at mRNA post-natal developmental changes, while the data from the Scnn1b-Tg line provides mRNA data that allows differential gene expression due to airway mucus obstruction to be queried. The data presented for the trachea is part of a larger body of work evaluating gene expression in whole lung, trachea, and purified macrophages. 24 Total tracheal samples were analyzed; three from each timepoint. In our manuscript, we were most interested in changes between WT and Scnn1b-Tg mice, however, the data can also be used to evaluate changes in gene expression across time (PND 0, 3, 10, and 42). It should be noted that a significant difference in RNA expression quality parameters was noted for the 10 day trachea data.
2014-09-11 | E-GEOD-47550 | biostudies-arrayexpress
Project description:The Drosophila tracheal system emerges as a favorable model for investigating the program of tubular morphogenesis. It is established in the embryo by post-mitotic cells, which also undergoes remodeling by modulating stem cells. Here we provide an analysis of a comprehensive cell atlas of Drosophila trachea using single-cell RNA-sequencing (scRNA-seq) and reveal cellular diversity and transcriptional profiles of tracheoblasts in Drosophila airway, which encompasses 9 major subtypes. Further evidences reveal transcription factors that are able to switch cell fate. The transcription factors, Peb, Bs, Kni, Sal and Cut are influenced by Notch signaling and determine cell identity. Moreover, Notch signaling that is responsible for the differentiation of tracheoblasts responds to protein glycosylation that is induced upon high sugar diet. Therefore, our study provides a transcriptomic atlas of tracheal development and regeneration, and suggests a glycosylation-responsive Notch signaling in cell fate determination.
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Project description:Nf-kB activity is associated with the key pathological features of chronic respiratory diseases including epithelial remodelling, excess mucous production, and submucosal gland hyperplasia. However, the role of Nf-kB activity in airway epithelial differentiation remains controversial. In the present study we demonstrate that Nf-kB adaptor protein Myd88 deficiency promotes increased airway submucosal gland abundance and abnormal epithelial differentiation in proximal adult airways. Abnormal airway differentiation was not developmentally determined, became exacerbated following acute lung injury, and did not involve altered epithelial proliferation or apoptosis. Instead, we demonstrate that tracheal Myd88 deficiency promotes upregulation of a unique gene expression profile that includes activation of alternate, Myd88-independent Nf-kB signalling. Finally, we show that these effects are not intrinsically maintained in vitro using an air-liquid interface epithelial culture. This finding indicates that Myd88 deficiency promotes adult airway remodelling by regulating non-epithelial, non-cell autonomous Nf-kB activity. 20 microarray samples of whole trachea RNA in total: 5 samples wildtype control tissue 5 samples Myd88 KO control tissue 5 samples wildtype 3 day polidocanol injury tissue 5 samples Myd88 KO 3 day polidocanol injury tissue
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Project description:The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 ± 15 pack-yr). Gene expression differences [fold-change >1.5, p< 0.01, Benjamini-Hochberg correction] were assessed with Affymetrix microarrays. 1,057 probe sets were differentially expressed in healthy smokers vs nonsmokers, representing >500 genes. Trachea gene expression was compared to an independent group of small airway epithelial samples (n=23 healthy nonsmokers, n=19 healthy smokers, 25 ± 12 pack-yr). The trachea epithelium is more sensitive to smoking, responding with 3-fold more differentially-expressed genes than small airway epithelium. The trachea transcriptome paralleled the small airway epithelium, with 156 of 167 (93%) genes that are significantly up- and down-regulated by smoking in the small airway epithelium showing similar direction and magnitude of response to smoking in the trachea. Trachea epithelium can be obtained without conscious sedation, representing a less invasive surrogate “canary” for smoking-induced changes in the small airway epithelium. This should prove useful in epidemiologic studies correlating gene expression with clinical outcome in assessing smoking-induced lung disease.
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