Cigarette smoking effect on pancreatic duct epithelial cells
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ABSTRACT:
PROVIDER: PRJNA407904 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of different expression of microRNAs in immortalized human pancreatic duct epithelial cells treated with cigarette smoke condensate. Cigarette smoking plays vital role in tumorigenesis and development of pancreatic ductal adenocarcinoma. Results provide insight in the machenisms involved in PDAC initiation and progression.
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Project description:Cigarette smoking is one of the major risk factors for Pancreatic Cancer. Our goal in this study is to investigate mechanistic link between smoking and pancreatic cancer stem cell (CSC) enrichment. We report that cigarette smoking augments pancreatic CSCs and this process occurs by the activation of Paf1/PD2, a major stem ness marker. We also report that the cigarette smoke activates Paf1/PD2 through nACHRα7-ERK1/2-FOSL1 signaling axis.
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Project description:Loss of CFTR function in the pancreatic duct leads to dysregulated luminal pH causing premature activation of digestive enzymes and tissue necrosis. Drastic alterations in pancreatic tissue architecture and cellular composition changes the microenvironment of the islets. Given that CFTR is expressed in the pancreatic ducts, we hypothesized that loss of functional CFTR impacts islet function by modifying the ductal secretome. To this end, we developed a long-term in vitro pancreatic duct epithelial cell culture system and polarized both WT and CFTR-KO (CF) ferret duct epithelial cells. We profiled the apical and basolateral secretome, and the cellular proteome of both WT and CF duct epithelium using quantitative mass spectrometry. Bioinformatic analysis of differentially secreted proteins mapped to their cognate receptors provided a list of putative paracrine interactions that affect islet function. Signaling pathways and upstream regulators that alter the secretome and cellular proteome profile were computationally mined to characterize disease causing mechanisms. In this study, we provide a proteomic roadmap of perturbed autocrine and paracrine signals from the CF pancreatic duct.
2021-05-27 | PXD025126 | Pride
Project description:Transcriptomic analysis of the effects of cigarette smoking on the gene expression in blood in humans
2012-10-01 | GSE23323 | GEO
Project description:Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. With the knowledge that the small airway epithelium is the earliest site of smoking-induced lung disease, and that the small airway epithelium is acutely sensitive to inhaled cigarette smoke with significant changes in the up- and down-regulation of hundreds of genes, we compared upper vs lower lobe gene expression in the small airway epithelium of the same cigarette smokers to determine if the gene expression patterns were similar or different. Active smokers (n=11) with early evidence of smoking-induced lung disease (normal spirometry but low diffusing capacity) underwent bronchoscopy and brushing of the small airway epithelium to compare upper vs lower lobe genome-wide gene expression assessed by microarray. Interestingly, cluster and principal component analysis demonstrated that, for each individual, the expression of the known small airway epithelium smoking-responsive genes were remarkably similar as upper vs lower lobe pairs, although, as expected, there were differences in the smoking-induced changes in gene expression from individual to individual. Thus, while there may be topographic differences in the distribution of cigarette smoke, sufficient smoke reaches the upper vs lower lobe small airway epithelium so that, within each smoker, the upper vs lower lobe gene expression are similar. These observations support the concept that the topographic differences in the occurrence of the smoking-induced lung diseases are likely secondary to topographic differences in the susceptibility of the upper vs lower lobes to cigarette smoke, not the topographic differences in distribution of inhaled cigarette smoke.
2017-03-08 | GSE26307 | GEO
Project description:Nine cigarette smoke condensates (CSCs) were produced under a standard ISO smoking machine regimen and one was produced by a more intense smoking machine regimen. These CSCs were used to treat primary normal human bronchial epithelial cells for 18 hours.
2009-09-24 | GSE18235 | GEO
Project description:The small airway epithelium (SAE), the first site of smoking-induced lung pathology, exhibits genome-wide changes in gene expression in response to cigarette smoking. Based on the increasing evidence that the epigenome can respond to external stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes compared to nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional output of these cells. Using genome-wide methylation analysis of SAE DNA of nonsmokers and smokers, the data identified 204 unique genes differentially methylated in SAE DNA of smokers compared to nonsmokers, with 67% of the regions with differential methylation occurring within 2 kb of the transcriptional start site. Among the genes with differential methylation were those related to metabolism, transcription, signal transduction and transport. For the differentially methylated genes, 34 exhibited a correlation with gene expression, 53% with an inverse correlation of DNA methylation with gene expression and 47% a direct correlation. These observations provide evidence that cigarette smoking alters the DNA methylation patterning of the SAE and that, for some genes, these changes are associated with the smoking-related changes in gene expression.
2013-08-05 | GSE43079 | GEO
Project description:The first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a “COPD-like” SAE transcriptome. SAE (10th-12th generation) was obtained via bronchoscopy of healthy nonsmokers, healthy smokers and COPD smokers and microarray analysis was used to identify differentially expressed genes. Individual responsiveness to smoking was quantified with an index representing the % of smoking-responsive genes abnormally expressed (ISAE), with healthy smokers grouped into “high” and “low” responders based on the proportion of smoking-responsive genes up- or down-regulated in each smoker. Smokers demonstrated significant variability in SAE transcriptome with ISAE ranging from 2.9 to 51.5%. While the SAE transcriptome of “low” responder healthy smokers differed from both “high” responders and smokers with COPD, the transcriptome of the “high” responder healthy smokers was indistinguishable from COPD smokers. The SAE transcriptome can be used to classify clinically healthy smokers into subgroups with lesser and greater responses to cigarette smoking, even though these subgroups are indistinguishable by clinical criteria. This identifies a group of smokers with a “COPD-like” SAE transcriptome.
2011-10-27 | GSE11784 | GEO
Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.
2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress
Project description:Cigarette smoking accounts for approximately one in five deaths in the United States. Previous genomic studies have primarily focused on gene level differential expression to identify related molecular signatures and pathways, but the genome-wide effects of smoking on alternative isoform regulation and posttranscriptional modulation have not yet been described. We attempted to fill this void by identifying smoking-associated isoform switches and their responsible splicing events and consequences using RNA-seq.
2021-12-01 | GSE171730 | GEO