Lung genes modification in elastase-induced emphysema following in utero nicotine exposure
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA704966 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13785865.fastq.gz | Fastqsanger.gz | |||
| SRR13785866.fastq.gz | Fastqsanger.gz | |||
| SRR13785867.fastq.gz | Fastqsanger.gz | |||
| SRR13785868.fastq.gz | Fastqsanger.gz | |||
| SRR13785869.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 35 |
Similar Datasets
Project description:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can prime the offspring to be more succetible to develop emphysema in adulthood Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). As a control, we used drinking water with 2% saccharin (control group). Pups born from nicotine-exposed or control mothers were intranasally instilled with elastase or saline at the age of 11 weeks and sacrificed at post-elastase day (ped) 21. Lungs were collected at ped21 and laser dissected to separate the emphysematous and normal-looking tissue from elastase-instilled lungs. The RNA was then extracted and submited to RNAseq analysis. We had 6 different groups: two for saline instilled animals (normal_control_saline (C-S), normal_nicotine-saline (N-S)), and for elastase-instilled animals we had 4 groups: 2 for emphysematous regions (emphysema_ControlElastase (eC-E) and emphysema_NicotineElastase(eN-E)) and 2 for normal regions (normal_ControlElastase(nC-E) and normal_NicotineElastase(nN-E)). Results: Nicotine upregulated zero and 46 genes and downregulated 2 and 29 in saline and elastase instilled respectivelly. Elastase upregulated zero and 3 and downregulated 1 and 1 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with differentially expressed genes due to nicotine-pretreatment in elastase instilled animals with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed downregulation of the several immune system related pathways, gamma-secretase proteolitic pathway, ubiquitin-proteasomal pathway, notch signaling pathway and others. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped21
2022-03-09 | GSE167568 | GEO
Project description:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can affect genetic profile in early ephysema Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). As a control, we used drinking water with 2% saccharin (control group). Pups born from nicotine-exposed or control mothers were intranasally instilled with elastase or saline at the age of 11 weeks and sacrificed at post-elastase day (ped) 3. Whole lung were collected at ped3 and total RNA was sequenced. We had 4 different groups: control_saline (C-S), control_elastase (C-E), nicotine_saline (N-S) and nicotine_elastase (N-E). ALl the groups had 3 replicas, except N-E group that had 5 different replicas. Results: At ped3 nicotine upregulated 219 and 2 and downregulated 2 and 109 genes in saline and elastase-instilled samples respectively. Elastase upregulated 723 and 439 and downregulated 116 and 77 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed many identical pathway activated by elastase instillation in both controls and nicotine-pretreated samples such as the cell cycle, DNA damage and cell adhesion, but also revieled the main difference in activation of the immune system between the controls and nicotine-pretreated samples. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped3
2022-03-09 | GSE167567 | GEO
Project description:Effect of in utero nicotine exposure and elastase instillation on transcriptomic profile at post-elastase day 3 in mice
| PRJNA704969 | ENA
Project description:Effect of in utero nicotine exposure and elastase instillation on transcriptomic profile at post-elastase day 21 in mice
| PRJNA704970 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-03-09 | GSE167569 | GEO
Project description:In a mouse model of elastase-induced emphysema, the effect of tetomilast against the emphysema development observed in C57BL/6J (C57) could be also detected in phosphodiesterase (PDE) 4D(+/+) but not in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) mice. Based on this result, we hypothesized that the difference in the efficacy of tetomilast among these strains of mice might result from the differences in the levels of the target molecules of tetomilast other than PDE4 in each mouse strain. To test this hypothesis, we used microarrays to compare the expression levels of genes in the lungs of each mouse strain. The expression profiling by array demonstrated that the levels of cyclin-dependent kinase inhibitor 1 (CDKN1a) in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) were higher than those in C57 and PDE4D(+/+).
2016-08-24 | GSE85962 | GEO
Project description:Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. Analysis of the accumulated eosinophils revealed differential transcriptomes between the mouse lungs of elastase-induced emphysema and ovalbumin-induced asthma., Eosinophil depletion alleviated elastase-induced emphysema. Notably, eosinophil-derived cathepsin L (CTSL) degraded the extracellular matrix (ECM), causing emphysema in the pulmonary tissue. Eosinophils were positively correlated with serum CTSL levels, which were increased in patients with emphysema than in those without emphysema. Collectively, these results suggest that CTSL expression in eosinophils plays an important role in ECM degradation and remodeling and is related to emphysema in patients with COPD. Therefore, eosinophil-derived CTSL may serve as a potential therapeutic target for patients with emphysema.
2023-10-17 | GSE237749 | GEO
Project description:In a mouse model of elastase-induced emphysema, the effect of tetomilast against the emphysema development observed in C57BL/6J (C57) could be also detected in phosphodiesterase (PDE) 4D(+/+) but not in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) mice. Based on this result, we hypothesized that the difference in the efficacy of tetomilast among these strains of mice might result from the differences in the levels of the target molecules of tetomilast other than PDE4 in each mouse strain. To test this hypothesis, we used microarrays to compare the expression levels of genes in the lungs of each mouse strain. The expression profiling by array demonstrated that the levels of cyclin-dependent kinase inhibitor 1 (CDKN1a) in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) were higher than those in C57 and PDE4D(+/+). Total RNAs were extracted from the lungs from naïve mice in each strain [C57, PDE4B(+/+), PDE4B(-/-), PDE4D(+/+), and PDE4D(-/)], and were used for microarray. In comparison with the expression levels of genes in C57, we retrieved the genes which expressed at the same levels in PDE4D(+/+), and at the different levels in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-).
2016-08-24 | E-GEOD-85962 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to address the consequences of in utero and early life nicotine exposure on alveolar phase of lung development in mice Methods: A mouse model of gestational and early life nicotine exposure was used in this study. Briefly, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and lactation (nicotine group). As a control, we used drinking water with 2% saccharin (saccharin group). Pups born from nicotine-exposed or control mothers were collected at different postnatal days (PNDs) and their lungs were subjected to RNAseq, western blot, histological and detailed stereological analysis. Results: Among 13 827 genes tested, nicotine treatment induced an upregulation of 2098 and downregulation of 1859. Pathway analysis performed with MetaCore software (https://portal.genego.com/) (threshold of 2 and p<0.05) identified several different pathways as upregulated upon nicotine exposure, namely cell cycle, epithelial to mesenchymal transition, stem cell related pathway, WNT signaling pathway, stromal-epithelial interaction, cell adhesion and DNA damage. Furthermore, majority of downregulated genes were associated with the immune system. Conclusions: Our results indicate that in utero and early life nicotine exposure induces extensive changes in gene expression following the birth of mice that reflects in accelerated kinetics of lung development. This effect, however, is transient, and not lomger detectable by pnd16. On the other hand, nicotine decreased proliferation and endothelial cell density detected at pnd16, thereby affecting on of two main cell lines involved in oxygen exchange. This results are important in the context of growing interest for nicotine patch replacement therapy and electronic cigarettes.
2020-02-11 | GSE102239 | GEO
Project description:To evaluate the effect of testosterone on the pathophysiology of COPD, we created porcine pancreas elastase (PPE)-induced emphysema mouse model in sham or orchiectomized (ORX) mice [sham/PBS, sham/PPE, ORX/PBS, and ORX/PPE]. We performed microarray analysis to compare the gene expression levels in the lungs of each mice group. The results demonstrated that the levels of genes encoding protease inhibitor activity in ORX/PPE mice were lower than those in sham/PPE mice.
2023-06-24 | GSE153148 | GEO