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MicroRNAs into body fluids from ten organs of mice exposed to cigarette smoke

ABSTRACT: The purpose of the present study was to validate the application of this epigenetic biomarker by using less invasive collection procedures.Using microarray analyses, we measured 1135 microRNAs in 10 organs and 3 body fluids of mice that were either unexposed or exposed to mainstream cigarette smoke for up to 8 weeks. The results obtained with selected miRNAs were validated by qPCR The lung was the main target effected by smoke (190 dysregulated miRNAs), followed by skeletal muscle (180), liver (138), blood serum (109), kidney (96), spleen (89), stomach (36), heart (33), bronchoalveolar lavage fluid (32), urine (27), urinary bladder (12), colon (5), and brain (0). Skeletal muscle, kidney, and lung were the most important sources of smoke-altered microRNAs in blood serum, urine, and bronchoalveolar lavage fluid, respectively

ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens

PROVIDER: GSE107962 | GEO | 2018/04/30

REPOSITORIES: GEO

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Project description:The objective of the study was to characterize the toxicity due to sub-chronic inhalation of test atmospheres from the heat not burn modified risk tobacco product (MRTP) - Tobacco Heating System version 2.2 (THS2.2) and to compare it to the toxicity inherent to the inhalation of mainstream smoke (MS) from the Reference Cigarette 3R4F (University_of_Kentucky, 2003). The 90-day nose-only inhalation study on Sprague-Dawley rats was performed according to the Organization for Economic Co-operation and Development (OECD) Test Guideline 413 (OECD, 2009), with special emphasis on histopathology of the respiratory tract, lung inflammation and additional systems toxicology-based assessment using transcriptomics. Animals were exposed to mainstream smoke from 3R4F reference cigarettes or THS2.2 mainstream aerosol at 3 target nicotine concentrations. The exposure regimen consisted of 6 hours a day, 5 days per week for 13 weeks, followed by 42 days recovery period. Exposure-related changes such as increased blood neutrophil count, decreased blood lymphocyte count, increased activity of alkaline phosphatase in serum and decreased cholesterol and glucose in serum were observed in 3R4F and THS2.2 exposed animals. Reduction in respiratory minute volume was significantly less pronounced in THS2.2 as compared to 3R4F-exposed groups. Histopathological findings in the respiratory tract including epithelial cell hyperplasia, squamous metaplasia, atrophy and accumulation of pigmented alveolar macrophages were significantly lower in THS2.2 than in 3R4F exposed groups. The degree of lung inflammation as indicated by accumulation of immune cells and pro-inflammatory and chemotactic cytokines in bronchioalveolar lavage fluid were significantly lower in THS2.2 as compared to 3R4F exposed groups. Transcriptomics data obtained from nasal epithelium and lung parenchyma showed concentration-dependent gene expression changes following 3R4F exposure that were much less pronounced in the THS2.2-exposed groups. In summary, the data indicates that the aerosol from THS2.2 did not cause additional toxicity as compared to the smoke from the 3R4F conventional cigarette. The toxicity on respiratory tract organs in THS2.2 exposed animals was much lower than in the rats exposed to 3R4F reference cigarette. Overall, the changes observed following exposure to THS2.2 can be considered mild and are very similar to previously published effects caused by nicotine only exposure at similar test atmosphere concentrations.

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MicroRNAs into body fluids from ten organs of mice exposed to cigarette smoke

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