Deregulated pulmonary growth hormones after intrauterine smoke exposure
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ABSTRACT:
PROVIDER: PRJNA281115 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Background: In utero smoke exposure is a recognized risk factor for impaired lung function development and a significant risk factor for airway disease. Despite intensive anti-tobacco campaigns the prevalence of smoking pregnant women has remained high requiring additional strategies to protect the offspring’s lung. To achieve this goal, it is critical to understand the mechanisms how disease risks are established in early life. Objective: To develop an animal model that recapitulates clinical findings in prenatally exposed children to allow the investigation of early molecular changes in the lung. Methods: Pregnant mice were exposed to active smoking from gestational day (GD) 2.5 until caesarean section or spontaneous delivery. After careful maternal characterization, we monitored weight development, lung function, and airway remodeling in offspring. mRNA/miRNA arrays were performed in fetal lungs (GD18.5), followed by network analyses, qPCR and histone analyses.
2019-09-25 | GSE67886 | GEO
Project description:Background: In utero smoke exposure is a recognized risk factor for impaired lung function development and a significant risk factor for airway disease. Despite intensive anti-tobacco campaigns the prevalence of smoking pregnant women has remained high requiring additional strategies to protect the offspring’s lung. To achieve this goal, it is critical to understand the mechanisms how disease risks are established in early life. Objective: To develop an animal model that recapitulates clinical findings in prenatally exposed children to allow the investigation of early molecular changes in the lung. Methods: Pregnant mice were exposed to active smoking from gestational day (GD) 2.5 until caesarean section or spontaneous delivery. After careful maternal characterization, we monitored weight development, lung function, and airway remodeling in offspring. mRNA/miRNA arrays were performed in fetal lungs (GD18.5), followed by network analyses, qPCR and histone analyses.
2019-09-25 | GSE67883 | GEO
Project description:Deregulated pulmonary growth hormones after intrauterine smoke exposure
| PRJNA281119 | ENA
Project description:Deregulated pulmonary growth hormones after intrauterine smoke exposure
| PRJNA281118 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-09-25 | GSE67888 | GEO
Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.
2020-11-01 | GSE136945 | GEO
Project description:Single cell RNA-sequencing (scRNAseq) of lung immune cells from mice exposed to room air or cigarette smoke, infected with influenza A virus. Room air saline controls are also included. This analysis facilitates a comparison of cigarette smoke-associated changes to the pulmonary immune environment at the level of individual leukocytes and stromal cells.
2022-01-03 | GSE186976 | GEO
Project description:Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats
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Project description:NOXO1 KO mice seem to be protected from cigarette smoke-induced emphysema and pulmonary hypertension. Since the molecular mechanisms are not clear yet, this microarray experiment should help to identify the molecular differences in these KO mice compared to the wild-type (WT), figuring out how the protection occurs. Since we believe that vascular altertions could not only be responsible for vascular remodeling but also the trigger for emphysema development, we microdissected pre-capillary vessels from WT and KO mice, both controls and smoke-exposed. In addition, alveolar septa were microdissected to investigate the alveolar changes.
2020-03-01 | GSE112287 | GEO
Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of lung toxicity in response to crystalline silica exposure. Nevertheless, the precise role of tobacco smoke exposure on the lung response to tobacco smoke exposure and the underlying mechanisms remain largely elusive. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary toxicity and the underlying molecular mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in rats exposed to air, crystalline silica, tobacco smoke, or crystalline silica plus tobacco smoke. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by tobacco smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to tobacco smoke, silica or a combination of both compared with the air exposed control rats.
2024-12-31 | GSE149286 | GEO