Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA380264 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:An In Vitro Versus In Vivo Toxicogenomics Investigation of Pre-natal Exposures to Tobacco Smoke
| PRJNA380260 | ENA
Project description:An In Vitro Versus In Vivo Toxicogenomics Investigation of Pre-natal Exposures to Tobacco Smoke [Dams, Prenatal offspring]
| PRJNA380263 | ENA
Project description:Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.
2016-10-12 | GSE82137 | GEO
Project description:Like tobacco smoking, habitual marijuana smoking causes numerous adverse pulmonary effects. However, the mechanisms of action involved, especially as compared to tobacco smoke, are still unclear. To uncover putative modes of action, this study employed a toxicogenomics approach to compare the toxicological pathways perturbed following exposure to marijuana and tobacco smoke condensate in vitro. Condensates of mainstream smoke from hand-rolled tobacco and marijuana cigarettes were similarly prepared using identical smoking conditions. Murine lung epithelial cells were exposed to low, medium and high concentrations of the smoke condensates for 6 hr. RNA was extracted immediately or after a 4-hr recovery period and hybridized to mouse whole genome microarrays. Tobacco smoke condensate (TSC) exposure was associated with changes in xenobiotic metabolism, oxidative stress, inflammation, and DNA damage response. These same pathways were also significantly affected following marijuana smoke condensate (MSC) exposure. Although the effects of the condensates were largely similar, dose-response analysis indicates that the MSC is substantially more potent than TSC. In addition, steroid biosynthesis, apoptosis, and inflammation pathways were more significantly affected following MSC exposure, whereas m-phase cell cycle pathways were more significantly affected following TSC exposure. MSC exposure also appeared to elicit more severe oxidative stress than TSC exposure, which may account for the greater cytotoxicity of MSC. This study shows that in general, MSC impacts many of the same molecular processes as TSC. However, subtle pathway differences can provide insight into the differential toxicities of the two complex mixtures.
2014-02-06 | GSE44603 | GEO
Project description:Like tobacco smoking, habitual marijuana smoking causes numerous adverse pulmonary effects. However, the mechanisms of action involved, especially as compared to tobacco smoke, are still unclear. To uncover putative modes of action, this study employed a toxicogenomics approach to compare the toxicological pathways perturbed following exposure to marijuana and tobacco smoke condensate in vitro. Condensates of mainstream smoke from hand-rolled tobacco and marijuana cigarettes were similarly prepared using identical smoking conditions. Murine lung epithelial cells were exposed to low, medium and high concentrations of the smoke condensates for 6 hr. RNA was extracted immediately or after a 4-hr recovery period and hybridized to mouse whole genome microarrays. Tobacco smoke condensate (TSC) exposure was associated with changes in xenobiotic metabolism, oxidative stress, inflammation, and DNA damage response. These same pathways were also significantly affected following marijuana smoke condensate (MSC) exposure. Although the effects of the condensates were largely similar, dose-response analysis indicates that the MSC is substantially more potent than TSC. In addition, steroid biosynthesis, apoptosis, and inflammation pathways were more significantly affected following MSC exposure, whereas m-phase cell cycle pathways were more significantly affected following TSC exposure. MSC exposure also appeared to elicit more severe oxidative stress than TSC exposure, which may account for the greater cytotoxicity of MSC. This study shows that in general, MSC impacts many of the same molecular processes as TSC. However, subtle pathway differences can provide insight into the differential toxicities of the two complex mixtures. Murine epithelial lung cells were exposed to tobacco smoke condensates (0, 25, 50, 90 μg/ml) or marijuana smoke condensates (0, 2.5, 5, 10 μg/ml) in serum-free medium for a six hour period. Following the six-hour exposure, cells were either harvested immediately or washed with phosphate-buffered saline and incubated in fresh serum-free medium for a four hour recovery period. Total RNA was extracted from the cells and hybridized against Universal Mouse Reference RNA (Agilent Technologies Canada, Inc.) to Agilent whole mouse genome microarray slides containing 44,000 transcripts. A LOWESS normalization was applied to expression results, and statistically significant genes were identified using the R library MAANOVA. Microarray results were validated by real time RT-PCR.
2014-02-06 | E-GEOD-44603 | biostudies-arrayexpress
Project description:Brain organoids (BO) enabled the investigation of human corticogenesis in-vitro with an increasing range of protocols achieving its remarkable recapitulation. However, we lack a resource gathering fetal cortex-specific gene co-expression patterns and their behavior in BO. We complement the current knowledge with a benchmarking of BO versus human corticogenesis, integrating: transcriptomes from in-house differentiated cortical BO (CBO), in-house processed human fetal brain samples, analysis of transcriptomes from different BO systems and of pre-natal cortical samples from the BrainSpan Atlas.
2022-12-31 | E-MTAB-11239 | biostudies-arrayexpress
Project description:Purpose: Globally, many jurisdictions are legalizing or decriminalizing cannabis, creating a potential public health issue that would benefit from experimental evidence to inform policy, government regulations, and user practices. Tobacco smoke exposure science has created a body of knowledge that demonstrates the conclusive negative impacts on respiratory health; similar knowledge remains to be established for cannabis. To address this unmet need, we performed in vitro functional and transcriptomic experiments with a human airway epithelial cell line (Calu-3) exposed to cannabis smoke, with tobacco smoke as a positive control. Results: We demonstrate that cannabis smoke induced functional and transcriptional responses that overlapped with tobacco smoke. Ontology and pathway analysis revealed that cannabis smoke induced DNA replication and oxidative stress responses. Functionally, cannabis smoke impaired epithelial cell barrier function, antiviral responses, and increased inflammatory mediator production. Our study reveals striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. LABA/GC intervention in airway epithelial cells exposed to cannabis smoke reduces levels of pro-inflammatory (CXCL8) and antiviral (CXCL10) mediators, while transcriptomic signatures of neutrophil mediated immunity and oxidative stress remain elevated. Conclusions: Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and user practices.
2020-01-28 | GSE125259 | 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
Project description:Our previous studies have shown that tobacco smoke exposure exacerbated the lung response to crystalline silica exposure in rats. The objective of the present study, a follow-up to our previous study, was to determine the effect of tobacco smoke exposure cessation on the lung response to crystalline silica exposure in the rats. Rats were exposed to air, crystalline silica (1 week followed by a 1 year progression/recovery period with no exposure), tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure), or crystalline silica (1 week) plus tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure). Lung toxicity was determined at the end of the 1-year progression/recovery period in all 4 groups of the rats. Silica exposure resulted in significant lung toxicity which was further exacerbated by tobacco smoke exposure in the rats. Cessation of cigarette smoke exposure did not result in reversal of the silica-induced lung toxicity despite exacerbation of the toxicity by tobacco smoke.
2024-12-31 | GSE155924 | GEO
Project description:Polycomb-mediated repression of Dkk-1 activates Wnt signaling and enhances tumorigenic potential of lung cancer cells following tobacco smoke exposure Keywords: tobacco Smoke, lung cancer, epigenetics
2009-04-10 | GSE13309 | GEO