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Whole DNA methylome profiling in mice exposed to secondhand smoke

ABSTRACT: A large body of evidence has linked secondhand smoke (SHS) to lung cancer in nonsmokers. Yet, the underlying mechanisms of SHS carcinogenicity in nonsmokers' lung cancer remain elusive. Recently, we have demonstrated a genotoxic mode of action for SHS, based on the ability of this carcinogen to induce adduct-driven mutagenesis in transgenic Big Blue® mice. In the present study, we have expanded this investigation to determine whether SHS can also cause epigenetic effects through aberrations of DNA methylation. Here, we have globally profiled DNA methylation in the lung of Big Blue® mice exposed to SHS for a duration of 4-months, both immediately after the termination of exposure and at several intervals post-exposure.

ORGANISM(S): Mus musculus

PROVIDER: GSE41421 | GEO | 2012/11/29

SECONDARY ACCESSION(S): PRJNA176927

REPOSITORIES: GEO

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Whole DNA methylome profiling in mice exposed to secondhand smoke

Project description:A large body of evidence has linked secondhand smoke (SHS) to lung cancer in nonsmokers. Yet, the underlying mechanisms of SHS carcinogenicity in nonsmokers' lung cancer remain elusive. Recently, we have demonstrated a genotoxic mode of action for SHS, based on the ability of this carcinogen to induce adduct-driven mutagenesis in transgenic Big Blue® mice. In the present study, we have expanded this investigation to determine whether SHS can also cause epigenetic effects through aberrations of DNA methylation. Here, we have globally profiled DNA methylation in the lung of Big Blue® mice exposed to SHS for a duration of 4-months, both immediately after the termination of exposure and at several intervals post-exposure. We have used a genome-wide microarray-based approach to catalogue DNA methylation profile in the lung of mice exposed to SHS and at various recovery periods from the time of exposure. Mice exposed to clean air, for comparable amount of times, were used as controls. Mice that were injected intraperitoneally with chronic doses of B(a)P (a powerful carcinogen in SHS) or DMSO (sham) were used for comparison purposes .

2012-11-29 | E-GEOD-41421 | biostudies-arrayexpress

Secondhand smoke induces liver steatosis through deregulation of genes involved in lipid metabolism.

Project description:In this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).

2020-03-23 | GSE139440 | GEO

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

2012-03-27 | GSE36810 | GEO

Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

2012-06-02 | GSE38409 | GEO

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs. Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).

2012-03-26 | E-GEOD-36810 | biostudies-arrayexpress

Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

Project description:SHS exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero SHS exposure and adult (19-23 weeks) OVA challenge in 23-week mouse lungs. Left lungs from Balb/c male and female mice were collected at 23 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on the gender differences and in-utero exposure status, there are 4 groups of mice, females and males, exposed in-utero to filtered-air or SHS. All were exposure to OVA (19-23 weeks). We extracted RNA from 4 animals from each group for microarray analysis (total N = 16 samples).

2012-06-01 | E-GEOD-38409 | biostudies-arrayexpress

Obesity and Poor Diet as Susceptibility Factors for Secondhand Smoke in Childhood Asthma

Project description:Aim 1: To investigate the effect of SHS exposure on asthma morbidity, systemic inflammation and oxidative stress among inner-city children with asthma. Hypotheses 1.Increasing SHS exposure will be associated with increases in asthma morbidity, systemic inflammation and oxidative stress. Aim 2: To determine if being overweight/obese modifies the effect of SHS exposure on respiratory symptoms, inflammation and oxidative stress responses among inner-city children with asthma.Hypothesis 2. SHS exposure will be associated with a worsened asthma and increases in systemic inflammation and oxidative stress among overweight/obese children compared to normal weight children. Aim 3: To determine if diet quality modifies the effect of SHS exposure on respiratory symptoms, inflammation and oxidative stress responses among inner-city children with asthma. Hypothesis 3. SHS smoke exposure will associated with worsened respiratory symptoms and increases in inflammation and oxidative stress among children with poor quality diet compared those with better quality diet inner-city children with asthma. (Diet will be assessed by dietary inflammatory index, healthy eating index, and additional serum markers proposed in this application).

2020-02-26 | ST001325 | MetabolomicsWorkbench

Alterations of DNA methylome during chemical carcinogenesis

Project description:Similar to other genotoxic polycyclic aromatic hydrocarbons (PAHs), benzo[a]pyrene (BaP) is known to produce stable DNA adducts and other DNA damage. BaP is a powerful carcinogen and can induce tumors in the accessory sex organs (including prostate) of rodents. In the present study, we have investigated the potential role of BaP as an epimutagen in vivo during chemical carcinogenesis. We have analyzed the DNA methylation profile, genome-wide, of seminal vesicles of Big Blue® mice exposed to chronic doses of BaP over a period of 6 weeks, both immediately after the termination of exposure and several weeks after-treatment in mice that have developed tumors on the accessory sex organs. Mice treated with chronic doses of DMSO (sham) were used as control.

2013-06-30 | GSE41422 | GEO

Threshold of Biologic Response of the Small Airway Epithelium to Low Levels of Tobacco Smoke

Project description:Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke.

2011-02-02 | GSE19667 | GEO

Identification of gene expression signature for cigarette smoke exposure response--from man to mouse.

Project description:Gene expression profiling data can be used in toxicology to assess both the level and impact of toxicant exposure, aligned with a vision of 21st century toxicology. Here, we present a whole blood-derived gene signature that can distinguish current smokers from either nonsmokers or former smokers with high specificity and sensitivity. Such a signature that can be measured in a surrogate tissue (whole blood) may help in monitoring smoking exposure as well as discontinuation of exposure when the primarily impacted tissue (e.g., lung) is not readily accessible. The signature consisted of LRRN3, SASH1, PALLD, RGL1, TNFRSF17, CDKN1C, IGJ, RRM2, ID3, SERPING1, and FUCA1. Several members of this signature have been previously described in the context of smoking. The signature translated well across species and could distinguish mice that were exposed to cigarette smoke from ones exposed to air only or had been withdrawn from cigarette smoke exposure. Finally, the small signature of only 11 genes could be converted into a polymerase chain reaction-based assay that could serve as a marker to monitor compliance with a smoking abstinence protocol.

2017-08-05 | E-MTAB-5279 | biostudies-arrayexpress

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