Exclusive heat-not-burn cigarette smoking alters the profile of circulating microRNAs.
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ABSTRACT:
PROVIDER: PRJNA975511 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24710334.fastq.gz | Fastqsanger.gz | |||
| SRR24710335.fastq.gz | Fastqsanger.gz | |||
| SRR24710336.fastq.gz | Fastqsanger.gz | |||
| SRR24710337.fastq.gz | Fastqsanger.gz | |||
| SRR24710338.fastq.gz | Fastqsanger.gz |
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Project description:Background. Traditional combustion cigarette (TCC) smoking is an established risk factor for several types of cancer and cardiovascular diseases. Circulating microRNAs (miRNAs) represent key molecules mediating pathogenetic mechanisms, and potential biomarkers for personalized risk assessment. Several transcriptomics studies have showed that TCC smoking globally changes the profile of circulating miRNAs. The use of heat-not-burn cigarettes (HNBCs) as alternative smoking devices is rising exponentially worldwide, with still unknown long-term effects on health. Comprehensive data on the circulating miRNA profile in chronic HNBC smokers are still lacking. Purpose. We aimed at defining the profile of circulating miRNAs in serum samples of chronic exclusive HNBC smokers, and identifying potentially pathogenetic circulating miRNA signatures. Results. Differential expression analysis revealed 101 miRNAs significantly modulated between groups (adjusted p<0.05), with a prevalence of circulating miRNA downregulation in smokers (only 20 miRNAs were upregulated in both groups of smokers). Head-to-head comparison revealed that 65 miRNAs were exclusively modulated in TCC, 26 miRNAs were commonly modulated in both smoker groups, and 10 miRNAs were exclusively modulated in HNBC samples, all versus NS. KEGG pathway analysis performed on target genes of the commonly modulated miRNAs returned cancer-associated and cardiovascular disease pathways. The application of stringent abundance and fold-change criteria to this list nailed down our functional bioinformatic analyses to a network where miR-25-3p and miR-221-3p are main hubs for cardiovascular- and cancer- related molecular pathways, respectively. Conclusions. Our results define for the first time a global miRNA profile in the serum of exclusive chronic HNBC smokers. Despite the globally lower extent of the differences observed, our data suggest a significant detrimental impact of HNBCs on circulating miRNAs.
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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.
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