Augmentation of Cystic Fibrosis Transmembrane Conductance Regulator Function in Human Bronchial Epithelial Cells via SLC6A14-Dependent Amino Acid Uptake. Implications for Treatment of Cystic Fibrosis
SLC6A14-mediated l-arginine transport has been shown to augment the residual anion channel activity of the major mutant, F508del-CFTR, in the murine gastrointestinal tract. It is not yet known if this transporter augments residual and pharmacological corrected F508del-CFTR in primary airway epitheli...
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Published in | American journal of respiratory cell and molecular biology Vol. 61; no. 6; pp. 755 - 764 |
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Main Authors | , , , , , , , , , , , , |
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American Thoracic Society
01.12.2019
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Abstract | SLC6A14-mediated l-arginine transport has been shown to augment the residual anion channel activity of the major mutant, F508del-CFTR, in the murine gastrointestinal tract. It is not yet known if this transporter augments residual and pharmacological corrected F508del-CFTR in primary airway epithelia. We sought to determine the role of l-arginine uptake via SLC6A14 in modifying F508del-CFTR channel activity in airway cells from patients with cystic fibrosis (CF). Human bronchial epithelial (HBE) cells from lung explants of patients without CF (HBE) and those with CF (CF-HBE) were used for H
-flux, airway surface liquid, and Ussing chamber studies. We used α-methyltryptophan as a specific inhibitor for SLC6A14. CFBE41o
, a commonly used CF airway cell line, was employed for studying the mechanism of the functional interaction between SLC6A14 and F508del-CFTR. SLC6A14 is functionally expressed in CF-HBE cells. l-arginine uptake via SLC6A14 augmented F508del-CFTR function at baseline and after treatment with lumacaftor. SLC6A14-mediated l-arginine uptake also increased the airway surface liquid in CF-HBE cells. Using CFBE41o cells, we showed that the positive SLC6A14 effect was mainly dependent on the nitric oxide (NO) synthase activity, nitrogen oxides, including NO, and phosphorylation by protein kinase G. These finding were confirmed in CF-HBE, as inducible NO synthase inhibition abrogated the functional interaction between SLC6A14 and pharmacological corrected F508del-CFTR. In summary, SLC6A14-mediated l-arginine transport augments residual F508del-CFTR channel function via a noncanonical, NO pathway. This effect is enhanced with increasing pharmacological rescue of F508del-CFTR to the membrane. The current study demonstrates how endogenous pathways can be used for the development of companion therapy in CF. |
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AbstractList | SLC6A14-mediated l-arginine transport has been shown to augment the residual anion channel activity of the major mutant, F508del-CFTR, in the murine gastrointestinal tract. It is not yet known if this transporter augments residual and pharmacological corrected F508del-CFTR in primary airway epithelia. We sought to determine the role of l-arginine uptake via SLC6A14 in modifying F508del-CFTR channel activity in airway cells from patients with cystic fibrosis (CF). Human bronchial epithelial (HBE) cells from lung explants of patients without CF (HBE) and those with CF (CF-HBE) were used for H
-flux, airway surface liquid, and Ussing chamber studies. We used α-methyltryptophan as a specific inhibitor for SLC6A14. CFBE41o
, a commonly used CF airway cell line, was employed for studying the mechanism of the functional interaction between SLC6A14 and F508del-CFTR. SLC6A14 is functionally expressed in CF-HBE cells. l-arginine uptake via SLC6A14 augmented F508del-CFTR function at baseline and after treatment with lumacaftor. SLC6A14-mediated l-arginine uptake also increased the airway surface liquid in CF-HBE cells. Using CFBE41o cells, we showed that the positive SLC6A14 effect was mainly dependent on the nitric oxide (NO) synthase activity, nitrogen oxides, including NO, and phosphorylation by protein kinase G. These finding were confirmed in CF-HBE, as inducible NO synthase inhibition abrogated the functional interaction between SLC6A14 and pharmacological corrected F508del-CFTR. In summary, SLC6A14-mediated l-arginine transport augments residual F508del-CFTR channel function via a noncanonical, NO pathway. This effect is enhanced with increasing pharmacological rescue of F508del-CFTR to the membrane. The current study demonstrates how endogenous pathways can be used for the development of companion therapy in CF. A study that determines the role of augmented cystic fibrosis (CF) transmembrane conductance regulator function in human bronchial epithelial cells through SLCA14-dependent amino acid uptake is featured. It offers details of the method of the study that uses airway surface liquid and observes a-methyltryptophan as a specific inhibitor for SLC6A14. It outlines the findings which indicate that SLC6A14-mediated l-arginine transport augments residual F508del-CFTR channel function via a noncanonical, enhancing pharmacological rescue of F508del-CFTR to the membrane. |
Author | Ahmadi, Saumel Du, Kai Gonska, Tanja Ip, Wan Wu, Yu-Sheng Xia, Sunny Li, Mingyuan Lew, Alexandria Di Paola, Michelle Bozoky, Zoltan Bear, Christine E Lloyd-Kuzik, Andrew Forman-Kay, Julie |
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Snippet | SLC6A14-mediated l-arginine transport has been shown to augment the residual anion channel activity of the major mutant, F508del-CFTR, in the murine... A study that determines the role of augmented cystic fibrosis (CF) transmembrane conductance regulator function in human bronchial epithelial cells through... |
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SubjectTerms | Airway management Amino Acid Transport Systems - antagonists & inhibitors Amino Acid Transport Systems - genetics Amino Acid Transport Systems - physiology Amino acids Arginine Arginine - metabolism Biological Transport Bronchi - cytology Bronchi - metabolism Cells, Cultured Cystic fibrosis Cystic Fibrosis - metabolism Cystic Fibrosis - therapy Cystic Fibrosis Transmembrane Conductance Regulator - deficiency Cystic Fibrosis Transmembrane Conductance Regulator - genetics Cystic Fibrosis Transmembrane Conductance Regulator - physiology Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Genes, Reporter Humans Lung diseases Nitric Oxide - metabolism Nitric Oxide Synthase Type II - antagonists & inhibitors Nitric Oxide Synthase Type II - metabolism Recombinant Proteins - metabolism Surface Properties Transduction, Genetic Tryptophan - analogs & derivatives Tryptophan - pharmacology |
Title | Augmentation of Cystic Fibrosis Transmembrane Conductance Regulator Function in Human Bronchial Epithelial Cells via SLC6A14-Dependent Amino Acid Uptake. Implications for Treatment of Cystic Fibrosis |
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