Transport of Ipratropium, an Anti-Chronic Obstructive Pulmonary Disease Drug, Is Mediated by Organic Cation/Carnitine Transporters in Human Bronchial Epithelial Cells: Implications for Carrier-Mediated Pulmonary Absorption

2010 ◽  
Vol 7 (1) ◽  
pp. 187-195 ◽  
Author(s):  
Toshimichi Nakamura ◽  
Takeo Nakanishi ◽  
Tsunemitsu Haruta ◽  
Yoshiyuki Shirasaka ◽  
John P. Keogh ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Organic Cation ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Pulmonary Absorption ◽  
Human Bronchial Epithelial Cells ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial

Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Alessia Santoro ◽  
Carlo Tomino ◽  
Giulia Prinzi ◽  
Palma Lamonaca ◽  
Vittorio Cardaci ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Tobacco Smoking ◽  
Nicotinic Receptors ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial

Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis. Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used. </P><P> Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. </P><P> New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported. Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation. Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.

scholarly journals Deducting MicroRNA-Mediated Changes Common in Bronchial Epithelial Cells of Asthma and Chronic Obstructive Pulmonary Disease—A Next-Generation Sequencing-Guided Bioinformatic Approach

2019 ◽  
Vol 20 (3) ◽  
pp. 553 ◽  
Author(s):  
Ming-Ju Tsai ◽  
Yu-Chen Tsai ◽  
Wei-An Chang ◽  
Yi-Shiuan Lin ◽  
Pei-Hsun Tsai ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Next Generation Sequencing ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Next Generation ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial ◽  
Generation Sequencing

Asthma and chronic obstructive pulmonary disease (COPD) are chronic airway inflammatory diseases that share some common features, although these diseases are somewhat different in etiologies, clinical features, and treatment policies. The aim of this study is to investigate the common microRNA-mediated changes in bronchial epithelial cells of asthma and COPD. The microRNA profiles in primary bronchial epithelial cells from asthma (AHBE) and COPD (CHBE) patients and healthy subjects (NHBE) were analyzed with next-generation sequencing (NGS) and the significant microRNA changes common in AHBE and CHBE were extracted. The upregulation of hsa-miR-10a-5p and hsa-miR-146a-5p in both AHBE and CHBE was confirmed with quantitative polymerase chain reaction (qPCR). Using bioinformatic methods, we further identified putative targets of these microRNAs, which were downregulated in both AHBE and CHBE: miR-10a-5p might suppress BCL2, FGFR3, FOXO3, PDE4A, PDE4C, and PDE7A; miR-146a-5p might suppress BCL2, INSR, PDE4D, PDE7A, PDE7B, and PDE11A. We further validated significantly decreased expression levels of FOXO3 and PDE7A in AHBE and CHBE than in NHBE with qPCR. Increased serum miR-146a-5p level was also noted in patients with asthma and COPD as compared with normal control subjects. In summary, our study revealed possible mechanisms mediated by miR-10a-5p and miR-146a-5p in the pathogenesis of both asthma and COPD. The findings might provide a scientific basis for developing novel diagnostic and therapeutic strategies.

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