Version 1
: Received: 13 May 2024 / Approved: 14 May 2024 / Online: 14 May 2024 (14:57:57 CEST)
How to cite:
Mirra, D.; Esposito, R.; Spaziano, G.; Rafaniello, C.; Panico, F.; Squillante, A.; Falciani, M.; Roviezzo, F.; Gallelli, L.; Cione, E.; D’Agostino, B. Cigarette Smoke Exposure and microRNA in Human Alveolar Macrophages: A Pilot Study. Preprints2024, 2024050961. https://doi.org/10.20944/preprints202405.0961.v1
Mirra, D.; Esposito, R.; Spaziano, G.; Rafaniello, C.; Panico, F.; Squillante, A.; Falciani, M.; Roviezzo, F.; Gallelli, L.; Cione, E.; D’Agostino, B. Cigarette Smoke Exposure and microRNA in Human Alveolar Macrophages: A Pilot Study. Preprints 2024, 2024050961. https://doi.org/10.20944/preprints202405.0961.v1
Mirra, D.; Esposito, R.; Spaziano, G.; Rafaniello, C.; Panico, F.; Squillante, A.; Falciani, M.; Roviezzo, F.; Gallelli, L.; Cione, E.; D’Agostino, B. Cigarette Smoke Exposure and microRNA in Human Alveolar Macrophages: A Pilot Study. Preprints2024, 2024050961. https://doi.org/10.20944/preprints202405.0961.v1
APA Style
Mirra, D., Esposito, R., Spaziano, G., Rafaniello, C., Panico, F., Squillante, A., Falciani, M., Roviezzo, F., Gallelli, L., Cione, E., & D’Agostino, B. (2024). Cigarette Smoke Exposure and microRNA in Human Alveolar Macrophages: A Pilot Study. Preprints. https://doi.org/10.20944/preprints202405.0961.v1
Chicago/Turabian Style
Mirra, D., Erika Cione and Bruno D’Agostino. 2024 "Cigarette Smoke Exposure and microRNA in Human Alveolar Macrophages: A Pilot Study" Preprints. https://doi.org/10.20944/preprints202405.0961.v1
Abstract
Cigarette smoke (CS) is a major driver of many respiratory diseases including chronic obstructive pulmonary disease (COPD) and non-small cell lung cancer (NSCLC). Tobacco causes oxidative stress, impaired phagocytosis of alveolar macrophages (AMs), and alterations in gene expression in the lungs of smokers. MicroRNAs (miRNAs) are small non-coding RNAs that influence several bi-ological processes and interfere with several regulatory pathways. The purpose of this study was to assess the effect of active CS on miRNAs expression in AMs obtained from bronchoalveolar lavage (BAL) of ever- or never-smoker subjects and patients with COPD or NSCLC. BAL specimens were collected from 43 sex-matched subjects to determine the expression of has-miR-34a-5p, 17-5p, 16-5p, 106a-5p, 223-5p, and 20a-5p before and after in vitro CS exposure by RT-PCR. In addition, bioin-formatic analysis of miRNAs target genes linked to inflammation was performed. Distinct and common miRNA expression profiles were identified in response to CS, suggesting their possible role in smoking-related diseases. It is noteworthy that, following exposure to CS, the expression levels of hsa-miR-34a-5p and 17-5p in both ever- or never-smokers, 106a-5p in never-smokers and 20a-5p in ever-smokers, shifted towards those found in individuals with COPD, suggesting them like a risk factor in developing this lung condition. Moreover, we identified miRNA targets involved in the immune system or AMs property regulation using in silico analysis. In conclusion, our study iden-tified miRNA signatures in AMs exposed to CS, indicating that CS is an important driver of epige-netic changes that contribute to the onset of various lung diseases.
Keywords
microRNAs; alveolar macrophages; cigarette smoke; COPD; lung cancer
Subject
Medicine and Pharmacology, Medicine and Pharmacology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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