Nicotine transport in lung and non-lung epithelial cells

Takano, Mikihisa; Kamei, Hidetaka; Nagahiro, Machi; Kawami, Masashi; Yumoto, Ryoko

doi:10.1016/j.lfs.2017.08.030

Cited by 15 publications

(7 citation statements)

References 22 publications

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“…The K m value (3.3 μ m ) of MTX uptake may indicate the involvement of RFC in MTX uptake in the presence of EDTA. On the other hand, the estimated uptake clearance (approximately 0.28 μl/mg protein per min) seems to be very low compared to other uptake systems such as nicotine uptake (approximately 12 μl/mg protein per min when estimated from our previous results) in H441 cells . Such a low MTX uptake activity was also observed in other cells such as hepatoma cell line Huh 7 and mouse cultured alveolar epithelial cells .…”

Section: Discussionsupporting

confidence: 40%

“…On the other hand, the estimated uptake clearance (approximately 0.28 ll/mg protein per min) seems to be very low compared to other uptake systems such as nicotine uptake (approximately 12 ll/mg protein per min when estimated from our previous results) in H441 cells. [32] Such a low MTX uptake activity was also observed in other cells such as hepatoma cell line Huh 7 and mouse cultured alveolar epithelial cells. [33,34] As the retention of intracellular MTX is increased by the formation of its polyglutamates, [35] MTX-induced toxicity may occur even if the uptake activity is low.…”

Section: Discussionmentioning

confidence: 63%

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Reduced folate carrier-mediated methotrexate transport in human distal lung epithelial NCl-H441 cells

Kawami

Honda

Miyamoto

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives We had previously found that reduced folate carrier (RFC; SLC19A1) is mainly involved in an influx of transport of methotrexate (MTX), a folate analogue, using alveolar epithelial A549 cells. Therefore, we examined MTX uptake in NCl‐H441 (H441) cells, another in vitro alveolar epithelial model, focusing on the localization of RFC in the present study. Methods Transport function of RFC in H441 cells was studied using [3H]MTX. Key findings The uptake of MTX was increased remarkably after pretreatment of the cell monolayer with ethylenediaminetetraacetic acid (EDTA) in H441 cells but not in A549 cells, indicating the contribution of the basolaterally located transporter. In addition, folic acid and thiamine monophosphate, RFC inhibitors, inhibited the uptake of MTX from the basolateral side of the H441 cells. In order to compare the function of RFC on the apical and basolateral sides of the cells, the uptake of MTX from each side was examined using a Transwell chamber. Intracellular MTX amounts from the basolateral side were found to be significantly higher than those from the apical side. Conclusions These findings suggest that the distribution of MTX in the lung alveolar epithelial cells may be mediated by basolaterally located RFC in alveolar epithelial cells.

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Section: Discussionsupporting

confidence: 40%

Section: Discussionmentioning

confidence: 63%

Reduced folate carrier-mediated methotrexate transport in human distal lung epithelial NCl-H441 cells

Kawami

Honda

Miyamoto

et al. 2019

Journal of Pharmacy and Pharmacology

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“…Among these toxic components, nicotine is the primary active substance of tobacco [ 7 ]. Nicotine can be rapidly absorbed from the oral mucosa and respiratory tract, inhaled into the lungs, and rapidly absorbed in the alveoli [ 8 , 9 , 10 , 11 ]. In addition, nicotine can also be absorbed through the skin and the gastrointestinal tract [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Cigarette Smoke Exposure on the Gut Microbiota and Liver Transcriptome in Mice Reveal Gut–Liver Interactions

Meng

Xing

et al. 2022

IJMS

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Cigarette smoke exposure has a harmful impact on health and increases the risk of disease. However, studies on cigarette-smoke-induced adverse effects from the perspective of the gut–liver axis are lacking. In this study, we evaluated the adverse effects of cigarette smoke exposure on mice through physiological, biochemical, and histopathological analyses and explored cigarette-smoke-induced gut microbiota imbalance and changes in liver gene expression through a multiomics analysis. We demonstrated that cigarette smoke exposure caused abnormal physiological indices (including reduced body weight, blood lipids, and food intake) in mice, which also triggered liver injury and induced disorders of the gut microbiota and liver transcriptome (especially lipid metabolism). A significant correlation between intestinal bacterial abundance and the expression of lipid-metabolism-related genes was detected, suggesting the coordinated regulation of lipid metabolism by gut microbiota and liver metabolism. Specifically, Salmonella (harmful bacterium) was negatively and positively correlated with up- (such as Acsl3 and Me1) and downregulated genes (such as Angptl4, Cyp4a12a, and Plin5) involved in lipid metabolism, while Ligilactobacillus (beneficial bacterium) showed opposite trends with these genes. Our results clarified the key role of gut microbiota in liver damage and metabolism and improved the understanding of gut–liver interactions caused by cigarette smoke exposure.

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“…1). More recently, Takano et al 29,30) reported that a carrier-mediated transport system, which is sensitive to hydrophobic cationic compounds, may be involved in nicotine uptake by rat primary cultured alveolar epithelial cells and epithelial cancer cell line such as NCI-H441 and MCF-7. These lines of evidence clearly suggest the importance of specific transport system(s) on nicotine tissue disposition.…”

Section: Transport Mechanism Of Nicotine In Tis-suesmentioning

confidence: 99%

Impact of Nicotine Transport across the Blood–Brain Barrier: Carrier-Mediated Transport of Nicotine and Interaction with Central Nervous System Drugs

Tega

Yamazaki

Akanuma

et al. 2018

Biological & Pharmaceutical Bulletin

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Nicotine, an addictive substance, is absorbed from the lungs following inhalation of tobacco smoke, and distributed to various tissues such as liver, brain, and retina. Recent in vivo and in vitro studies suggest the involvement of a carrier-mediated transport process in nicotine transport in the lung, liver, and inner blood-retinal barrier. In addition, in vivo studies of influx and efflux transport of nicotine across the blood-brain barrier (BBB) revealed that blood-to-brain influx transport of nicotine is more dominant than brain-to-blood efflux transport of nicotine. Uptake studies in TR-BBB13 cells, which are an in vitro model cell line of the BBB, suggest the involvement of H/organic cation antiporter, which is distinct from typical organic cation transporters, in nicotine transport at the BBB. Moreover, inhibition studies in TR-BBB13 cells showed that nicotine uptake was significantly reduced by central nervous system (CNS) drugs, such as antidepressants, anti-Alzheimer's disease drugs, and anti-Parkinson's disease drugs, suggesting that the nicotine transport system can recognize these molecules. The cumulative evidence would be helpful to improve our understanding of smoking-CNS drug interaction for providing appropriate medication.

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Nicotine transport in lung and non-lung epithelial cells

Cited by 15 publications

References 22 publications

Reduced folate carrier-mediated methotrexate transport in human distal lung epithelial NCl-H441 cells

Reduced folate carrier-mediated methotrexate transport in human distal lung epithelial NCl-H441 cells

Effects of Cigarette Smoke Exposure on the Gut Microbiota and Liver Transcriptome in Mice Reveal Gut–Liver Interactions

Impact of Nicotine Transport across the Blood–Brain Barrier: Carrier-Mediated Transport of Nicotine and Interaction with Central Nervous System Drugs

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