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Oliynyk, Igor
Publications (9 of 9) Show all publications
Hussain, R., Oliynyk, I., Roomans, G. M. & Björkqvist, M. (2013). Modulation of ENaC, CFTR, and iNOS expression in bronchial epithelial cells after stimulation with Staphylococcus epidermidis (94B080) and Staphylococcus aureus (90B083). Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 121(9), 814-826
Open this publication in new window or tab >>Modulation of ENaC, CFTR, and iNOS expression in bronchial epithelial cells after stimulation with Staphylococcus epidermidis (94B080) and Staphylococcus aureus (90B083)
2013 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 121, no 9, p. 814-826Article in journal (Refereed) Published
Abstract [en]

Bacteria affect the respiratory epithelium, which is covered by airway surface liquid (ASL) and mucus. Ion concentrations in the ASL are determined by the cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial Na+ channel (ENaC). Neonatal sepsis is a major risk factor for subsequent pulmonary disease in preterm newborns. Predominating are coagulase-negative staphylococci (e.g., Staphylococccus epidermidis and Staphylococccus aureus). The aim of this study was to investigate modulation of CFTR, ENaC, mucins, proinflammatory cytokines, and inducible nitric oxide synthase (iNOS) in respiratory epithelial cells after S. epidermidis 94B080 and S. aureus 90B083 exposure. Bronchial epithelial cells were incubated with S. epidermidis 94B080 and S. aureus 90B083 (neonatal blood isolates) for 1-36h. Expression of CFTR, ENaC, iNOS, and mucins was analyzed by real-time PCR and Western blotting. Release of cytokines was analyzed by ELISA, and production of NO by the Griess assay. Expression of CFTR significantly decreased after 36h incubation with S. epidermidis and more prominently with S. aureus, whereas S. epidermidis caused a significant increase in the expression of - and -ENaC. Expression of iNOS increased, but NO was not detected. Both staphylococci caused a decrease in the intracellular Ca2+ concentration. S. aureus induced increased secretion of IL-6, IL-8, and transforming nuclear factor (TNF)- in a time-dependent manner as compared with S. epidermidis. In conclusion, expression of ENaC, CFTR, and iNOS is modulated by exposure to S. aureus 90B083 and S. epidermidis 94B080. S. aureus is more potent in causing release of IL-6, IL-8, and TNF- by bronchial epithelial cells as compared with S. epidermidis. The mRNA expression for the mucus proteins MUC2, MUC5AC, and MUC5B could not be measured, neither in the presence nor in the absence of bacteria.

Place, publisher, year, edition, pages
Hoboken, USA: Wiley-Blackwell, 2013
Keywords
Airway epithelium, Staphylococcus aureus 90B083, Staphylococcus epidermidis 94B080, CFTR, ENaC, iNOS, cytokines
National Category
Medical and Health Sciences Immunology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-30514 (URN)10.1111/apm.12138 (DOI)000322757000003 ()23879620 (PubMedID)2-s2.0-84881558007 (Scopus ID)
Note

Funding Agencies:

Nyckelfonden of Örebro University Hospital 

Swedish Science Research Council 

Swedish Heart Lung Foundation 

Available from: 2013-08-30 Created: 2013-08-30 Last updated: 2018-05-21Bibliographically approved
Varelogianni, G., Hussain, R., Strid, H., Oliynyk, I., Roomans, G. M. & Johannesson, M. (2013). The effect of ambroxol on chloride transport, CFTR and ENaC in cysticfibrosis airway epithelial cells. Cell Biology International, 37(11), 1149-1156
Open this publication in new window or tab >>The effect of ambroxol on chloride transport, CFTR and ENaC in cysticfibrosis airway epithelial cells
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2013 (English)In: Cell Biology International, ISSN 1065-6995, E-ISSN 1095-8355, Vol. 37, no 11, p. 1149-1156Article in journal (Refereed) Published
Abstract [en]

Ambroxol, a mucokinetic anti-inflammatory drug, has been used for treatment of cystic fibrosis (CF). The respiratoryepitheliumis covered by the airway surface liquid (ASL), the thickness and composition of which is determined by Cl efflux viathe cystic fibrosis transmembrane conductance regulator (CFTR) and Naþ influx via the epithelial Naþ channel (ENaC). In cellsexpressing wt-CFTR, ambroxol increased the Cl- conductance, but not the bicarbonate conductance of the CFTR channels.Weinvestigated whether treatment with ambroxol enhances chloride transport and/or CFTR and ENaC expression in CF airwayepithelial cells (CFBE) cells. CFBE cells were treated with 100 mM ambroxol for 2, 4 or 8 h. mRNA expression for CFTR andENaC subunits was analysed by real-time polymerase chain reaction (RT-PCR); protein expression was measured by Westernblot. The effect of ambroxol on Cl− transport was measured by Cl− efflux measurements with a fluorescent chloride probe.Ambroxol significantly stimulated Cl− efflux from CFBE cells (a sixfold increase after 8 h treatment), and enhanced theexpression of the mRNA of CFTR and a-ENaC, and of the CFTR protein. No significant difference was observed in b-ENaCafter exposure to ambroxol, whereasmRNA expression of g-ENaC was reduced. No significant effects of ambroxol on the ENaCsubunits were observed by Western blot. Ambroxol did not significantly affect the intracellular Ca2+ concentration.Upregulation of CFTR and enhanced Cl efflux after ambroxol treatment should promote transepithelial ion and watertransport, which may improve hydration of the mucus, and therefore be beneficial to CF-patients.

Place, publisher, year, edition, pages
Hoboken, USA: Wiley-Blackwell, 2013
Keywords
Airway epithelium, ambroxol, cystic fibrosis, Cl− efflux, CFTR; ENaC
National Category
Medical and Health Sciences Cell Biology
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-32769 (URN)10.1002/cbin.10146 (DOI)000325489500002 ()23765701 (PubMedID)2-s2.0-84885861654 (Scopus ID)
External cooperation:
Funder
Swedish Heart Lung FoundationSwedish Research Council
Note

Funding Agencies:

Swedish Science Research Council 

Available from: 2013-12-13 Created: 2013-12-13 Last updated: 2017-12-06Bibliographically approved
Oliynyk, I., Hussain, R., Amin, A., Johannesson, M. & Roomans, G. M. (2013). The effect of NO-donors on chloride efflux, intracellular Ca2+ concentration and mRNA expression of CFTR and ENaC in cystic fibrosis airway epithelial cells. Experimental and molecular pathology (Print), 94(3), 474-480
Open this publication in new window or tab >>The effect of NO-donors on chloride efflux, intracellular Ca2+ concentration and mRNA expression of CFTR and ENaC in cystic fibrosis airway epithelial cells
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2013 (English)In: Experimental and molecular pathology (Print), ISSN 0014-4800, E-ISSN 1096-0945, Vol. 94, no 3, p. 474-480Article in journal (Refereed) Published
Abstract [en]

Since previous studies showed that the endogenous bronchodilator, S nitrosglutathione (GSNO), caused amarked increase in CFTR-mediated chloride (Cl−) efflux and improved the trafficking of CFTR to the plasmamembrane, and that also the nitric oxide (NO)-donor GEA3162 had a similar, but smaller, effect on Cl− efflux, itwas investigatedwhether the NO-donor properties of GSNOwere relevant for its effect on Cl− efflux fromairwayepithelial cells. Hence, the effect of a number of other NO-donors, sodium nitroprusside (SNP), S-nitroso-Nacetyl-DL-penicillamine (SNAP), diethylenetriamine/nitric oxide adduct (DETA-NO), and diethylenetriamine/nitricoxide adduct (DEA-NONOate) on Cl− efflux from CFBE (ΔF508/ΔF508-CFTR) airway epithelial cells was tested.Cl− efflux was determined using the fluorescent N-(ethoxycarbonylmethyl)-6-methoxyquinoliniu bromide(MQAE)-technique. Possible changes in the intracellular Ca2+ concentration were tested by the fluorescent fluo-4method in a confocal microscope system. Like previously with GSNO, after 4 h incubation with the NO-donor, anincreased Cl− efflux was found (in the order SNAP > DETA-NO > SNP). The effect of DEA-NONOate on Cl− effluxwas not significant, and the compound may have (unspecific) deleterious effects on the cells. Again, as withGSNO, after a short (5 min) incubation, SNP had no significant effect on Cl− efflux. None of the NO-donors thathad a significant effect on Cl− efflux caused significant changes in the intracellular Ca2+ concentration. After 4 hpreincubation, SNP caused a significant increase in the mRNA expression of CFTR. SNAP and DEA-NONOatedecreased the mRNA expression of all ENaC subunits significantly. DETA-NO caused a significant decrease only inα-ENaC expression. After a short preincubation, none of the NO-donors had a significant effect, neither on theexpression of CFTR, nor on that of the ENaC subunits in the presence and absence of L-cysteine. It can be concludedthat the effect of GSNO on Cl−efflux is, at least in part, due to its properties as an NO-donor, and the effect is likely tobe mediated by CFTR, not by Ca2+-activated Cl− channels.

Place, publisher, year, edition, pages
Maryland Heights, USA: Elsevier, 2013
Keywords
Nitric oxide donors, Cystic fibrosis, Airway epithelium, CFTR, ENaC, Calcium
National Category
Medical and Health Sciences Cell Biology
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-32767 (URN)10.1016/j.yexmp.2013.03.003 (DOI)000319535900008 ()23523754 (PubMedID)2-s2.0-84876344605 (Scopus ID)
Funder
Swedish Heart Lung FoundationNIH (National Institute of Health)Swedish Research Council
Available from: 2013-12-13 Created: 2013-12-13 Last updated: 2017-12-06Bibliographically approved
Oliynyk, I. (2010). Advances in Pharmacological Treatment of Cystic Fibrosis. (Doctoral dissertation). Örebro: Örebro university
Open this publication in new window or tab >>Advances in Pharmacological Treatment of Cystic Fibrosis
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Cystic fibrosis (CF) is an inborn, hereditary disease, due to mutations in the gene for a cAMP-activated chloride (Cl-) channel, the cystic fibrosis transmembrane conductance regulator (CFTR). As a result of impaired ion and water transport,the airway mucus is abnormally viscous, which leads to bacterial colonization.Recurrent infections and inflammation result in obstructive pulmonary disease.Similar changes in the pancreas lead to pancreatic insufficiency.Several compounds have been tested to improve transepithelial ion transport in CF patients, either via activation of the mutant CFTR, or via stimulation of alternative chloride channels. The main purpose of this thesis was to find substances that might correct the defective ion transport in epithelial cells in CFand could be useful for the pharmacological treatment of CF patients. Long-term treatment with the macrolide antibiotic azithromycin (AZM)improved clinical parameters and lung function in CF patients and increased Cl- transport in CF bronchial epithelial cells (CFBE) (Paper I); although mRNA expression of the CFTR gene remained unchanged.In contrast, pre-exposure to the mucolytic antioxidant N-acetylcysteine (NAC) increased CFTR protein expression and was associated with increased Cl- efflux from CFBE cells (Paper II). Clinical trials of this substance might be warranted. Duramycin has been the subject of clinical trials that finished in June2009. Up till now, no results from this study are available. The effect of this substance on Cl- efflux from three CF and three non-CF cell lines (Paper III) was disappointing. An effect was found only in CFBE cells, the effect was minimal, occurred in a narrow concentration range, and was not associated with an increase in the intracellular calcium concentration [Ca2+]i. The fact that NO-donors stimulated Cl- efflux from CFBE cells (but did notchange [Ca2+]i) after several hours of preincubation suggests that these substances may be a potentially interesting group of compounds for the treatment of CF (Paper IV). A model for the effect of NO-donors on Cl- efflux is presented.

Abstract [sv]

Cystisk fibros (CF) är en medfödd, ärftlig, sjukdom, som förorsakas av en mutation i en gen som innehåller koden för en kloridkanal som aktiveras av cykliskt AMP (cystic fibrosis transmembrane conductance regulator, CFTR). Som en följd av otillräcklig transport av joner och vatten är slemmet i luftvägarna onormalt segt, vilket leder till att det koloniseras av bakterier. Upprepade infektioneroch inflammation av luftvägarna leder slutligen till obstruktiv lungsjukdom.Liknande förändringar i bukspottkörteln leder till att också detta organ inte fungerar. Flera kemiska ämnen har testats för sin förmåga att förbättra jontransporten över epitelet hos CF-patienter. Detta skulle kunna göras antingen genom aktivering av det muterade CFTR-proteinet, eller genom stimulering av alternativa kloridkanaler. Huvudsyftet med den forskning som beskrivs i denna avhandling var att hitta kemiska substanser som skulle kunna korrigera den defekta jontransporten i epitelceller hos CF-patienter, och därför vara nyttiga för behandlingen av patienterna. Behandling under längre tid med azithromycin (AZM), ett makrolidantibiotikum,förbättrade CF-patienternas kliniska status och lungfunktion,samt ökade kloridutflödet från CF bronkialepitelceller (CFBE-celler) (Arbete I).Däremot ändrades inte uttrycket av mRNA för CFTR-genen. I kontrast till detta ökade uttrycket av CFTR-proteinet om CFBE-cellerna utsattes för den slemlösande anti-oxidanten N-acetylcystein (NAC), vilket ledde till ökat kloridutflöde från denna cellinje (Arbete II). Det vore rimligt att utföra kliniska prövningar av detta ämne. Duramycin har testats i kliniska prov som slutade i juni 2009, men några resultatfrån dessa prov har inte offentliggjorts än. Effekten av detta ämne på kloridutflödet från tre CF-cellinjer och tre icke-CF cellinjer (Arbete III) var en besvikelse. Duramycin hade endast effekt på CFBE-celler, effekten var mycket liten, förekom endast i ett litet koncentrationsområde av duramycin, och var inte kopplad till en ökning av den intracellulära kalciumkoncentrationen [Ca2+]i. Att ämnen som avger kväveoxid (NO) stimulerade kloridutflödet från CFceller (men inte påverkade [Ca2+]i) efter några timmar, visar att denna grupp av ämnen kan vara potentiellt intressant för behandlingen av CF (arbete IV). En modell för effekten av NO på kloridtransporten i CF-celler presenteras.

Place, publisher, year, edition, pages
Örebro: Örebro university, 2010. p. 88
Series
Örebro Studies in Medicine, ISSN 1652-4063 ; 50
Keywords
Cystic fibrosis, CFTR, chloride transport, N-acetylcysteine, NO-donors, duramycin, intracellular calcium, azithromycin
National Category
Medical and Health Sciences
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-12424 (URN)978-91-7668-773-4 (ISBN)
Public defence
2010-12-17, Konferensrum Hjälmaren, USÖ, M-huset, S. Grev Rosengatan, Örebro, 09:15
Opponent
Supervisors
Available from: 2010-11-12 Created: 2010-11-08 Last updated: 2017-10-17Bibliographically approved
Oliynyk, I., Varelogianni, G., Roomans, G. M. & Johannesson, M. (2010). Effect of duramycin on chloride transport and intracellular calcium concentration in cystic fibrosis and non-cystic fibrosis epithelia. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 118(12), 982-990
Open this publication in new window or tab >>Effect of duramycin on chloride transport and intracellular calcium concentration in cystic fibrosis and non-cystic fibrosis epithelia
2010 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 118, no 12, p. 982-990Article in journal (Refereed) Published
Abstract [en]

The lantibiotic duramycin (Moli1901, Lancovutide) has been suggested as a drug of choice in the treatment for cystic fibrosis (CF). It has been proposed that duramycin may stimulate chloride secretion through Ca2+-activated Cl channels (CaCC). We investigated whether duramycin exhibited any effect on Cl efflux and intracellular Ca2+ concentration ([Ca2+]i) in CF and non-CF epithelial cells. Duramycin did stimulate Cl efflux from CF bronchial epithelial cells (CFBE) in a narrow concentration range (around 1 μM). However, 100 and 250 μM of duramycin inhibited Cl efflux from CFBE cells. An inhibitor of the CF transmembrane conductance regulator (CFTRinh-172) and a blocker of the capacitative Ca2+ entry, gadolinium chloride, inhibited the duramycin-induced Cl efflux. No effect on Cl efflux was observed in non-CF human bronchial epithelial cells (16HBE), human airway submucosal gland cell line, human pancreatic epithelial cells, CF airway submucosal gland epithelial cells, and CF pancreatic cells. The [Ca2+]i was increased by 3 μM duramycin in 16HBE cells, but decreased after 1, and 3 μM of duramycin in CFBE cells. The results suggest that the mechanism responsible for the stimulation of Cl efflux by duramycin is mainly related to unspecific changes of the cell membrane or its components rather than to effects on CaCC.

Place, publisher, year, edition, pages
New York, USA: John Wiley & Sons, 2010
Keywords
Duramycin, cystic fibrosis, airway epithelium, chloride efflux
National Category
Medical and Health Sciences Immunology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-12442 (URN)10.1111/j.1600-0463.2010.02680.x (DOI)000284317500010 ()21091780 (PubMedID)2-s2.0-78649506897 (Scopus ID)
Available from: 2010-11-11 Created: 2010-11-11 Last updated: 2018-04-19Bibliographically approved
Varelogianni, G., Oliynyk, I., Roomans, G. M. & Johannesson, M. (2010). The effect of N-acetylcysteine on chloride efflux from airway epithelial cells. Cell Biology International, 34(3), 245-252
Open this publication in new window or tab >>The effect of N-acetylcysteine on chloride efflux from airway epithelial cells
2010 (English)In: Cell Biology International, ISSN 1065-6995, E-ISSN 1095-8355, Vol. 34, no 3, p. 245-252Article in journal (Refereed) Published
Abstract [en]

Defective chloride transport in epithelial cells increases mucus viscosity and leads to recurrent infections with high oxidative stress in patients with CF (cystic fibrosis). NAC (N-acetylcysteine) is a well known mucolytic and antioxidant drug, and an indirect precursor of glutathione. Since GSNO (S-nitrosoglutathione) previously has been shown to be able to promote Cl efflux from CF airway epithelial cells, it was investigated whether NAC also could stimulate Cl efflux from CF and non-CF epithelial cells and through which mechanisms. CFBE (CF bronchial epithelial cells) and normal bronchial epithelial cells (16HBE) were treated with 1 mM, 5 mM, 10 mM or 15 mM NAC for 4 h at 37°C. The effect of NAC on Cl transport was measured by Cl efflux measurements and by X-ray microanalysis. Cl efflux from CFBE cells was stimulated by NAC in a dose-dependent manner, with 10 mM NAC causing a significant increase in Cl efflux with nearly 80% in CFBE cells. The intracellular Cl concentration in CFBE cells was significantly decreased up to 60% after 4 h treatment with 10 mM NAC. Moreover immunocytochemistry and Western blot experiments revealed expression of CFTR channel on CFBE cells after treatment with 10 mM NAC. The stimulation of Cl efflux by NAC in CF airway epithelial cells may improve hydration of the mucus and thereby be beneficial for CF patients.

Place, publisher, year, edition, pages
London: Portland Press Ltd, 2010
Keywords
airway epithelium, chloride transport, cystic fibrosis, N-acetylcysteine, Medical cell biology, Morphology, cell biology, pathology
National Category
Cell and Molecular Biology Medical and Health Sciences Cell and Molecular Biology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-12451 (URN)10.1042/CBI20090007 (DOI)000277391600002 ()
Note

Georgia Varelogianni, Igor Oliynyk, Godfried M Roomans are also affiliated w. Department of Medical Cell Biology, Uppsala University, Box 571, SE-75123 Uppsala, Sweden

Available from: 2010-11-12 Created: 2010-11-12 Last updated: 2018-04-19Bibliographically approved
Oliynyk, I., Varelogianni, G., Schalling, M., Stenkvist Asplund, M., Roomans, G. M. & Johannesson, M. (2009). Azithromycin increases chloride efflux from cystic fibrosis airway epithelial cells. Experimental Lung Research, 35(3), 210-221
Open this publication in new window or tab >>Azithromycin increases chloride efflux from cystic fibrosis airway epithelial cells
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2009 (English)In: Experimental Lung Research, ISSN 0190-2148, E-ISSN 1521-0499, Vol. 35, no 3, p. 210-221Article in journal (Refereed) Published
Abstract [en]

It was investigated whether azithromycin (AZM) stimulates chloride (Cl−) efflux from cystic fibrosis (CF) and non-CF airway epithelial cells, possibly secondary to up-regulation of the multidrug resistance protein (MDR). CF and non-CF human airway epithelial cell lines (CFBE and 16HBE) were treated with 0.4, 4, and 40 μ g/mL AZM for 4 days. Cl− efflux was explored in the presence or absence of specific inhibitors of CFTR and alternative Cl−  channels. Six CF patients received AZM (500 mg daily) for 6 months. The percentage of predicted forced vital capacity (FVC%), forced expiratory volume (FEV1%), and the number of acute exacerbations were compared before and after treatment. Nasal biopsies were taken before and after treatment, and mRNA expression of MDR and CFTR was determined by in situ hybridization. A significant dose-dependent increase of Cl− efflux from CFBE cells (but not from 16HBE cells) was observed after AZM treatment. A CFTR inhibitor significantly reduced AZM-stimulated Cl−  efflux from CFBE cells. A significant improvement in FEV1%, and fewer exacerbations were observed. AZM treatment did not affect mRNA expression of MDR and CFTR. The stimulation of Cl− efflux could be part of the explanation for the clinical improvement seen among the patients.

Place, publisher, year, edition, pages
Taylor & Francis, 2009
Keywords
azithromycin, chloride transport, cystic fibrosis, lung function, Morphology, Medical cell biology, pathology
National Category
Medical and Health Sciences Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-12440 (URN)10.1080/01902140802534967 (DOI)000264750200004 ()19337904 (PubMedID)2-s2.0-67149144260 (Scopus ID)
Available from: 2010-11-11 Created: 2010-11-11 Last updated: 2017-12-12Bibliographically approved
Oliynyk, I., Amin, A., Johannesson, M., Gaston, B. & Roomans, G. M.Effect of NO-donors on chloride efflux and intracellular Ca2+ concentration in cystic fibrosis airway epithelial cells.
Open this publication in new window or tab >>Effect of NO-donors on chloride efflux and intracellular Ca2+ concentration in cystic fibrosis airway epithelial cells
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(English)Manuscript (preprint) (Other academic)
Abstract [en]

Previous studies have shown that the endogenous bronchodilator, S-nitrosglutathione (GSNO), causes a 4–fold increase in CFTR-mediated chloride (Cl) efflux and improves the trafficking of CFTR to the plasma membrane. The NO-donor GEA3162 had a similar, but smaller, effect on Cl efflux. In order to investigate whether the NO-donor properties of GSNO were relevant for its effect on Cl efflux from airway epithelial cells, the effect of a number of other NO-donors (SNP, SNAP, DETA-NO, and DEA-NONOate) on Cl efflux from CFBE (DF508/DF508) airway epithelial cells was tested. Cl efflux was determined using the fluorescent MQAE-technique. Possible changes in the intracellular Ca2+ concentration were tested by the fluorescent fluo-4 method in a confocal microscope system. Like GSNO, SNP had no immediate effect on Cl efflux, but after 4h incubation with the NO-donor, an increased Cl efflux was found (in the order SNAP > DETA-NO > DEA- NONOate > SNP). The effect of DEA-NONOate on Cl efflux was not significant, and the compound may have (unspecific) deleterious effects on the CFBE cells. None of the compounds that caused significant Cl efflux caused significant changes in the intracellular Ca2+ concentration. It is concluded that the effect of GSNO is, at least in part, due to its properties as an NO-donor, and that the effect is likely to be mediated by the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), not on Ca2+-activated Cl channels.

Keywords
Nitric oxide donors, cystic fibrosis, airway epithelium, chloride channels, medical cell biology
National Category
Medical and Health Sciences
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-12446 (URN)
Available from: 2010-11-11 Created: 2010-11-11 Last updated: 2017-10-17Bibliographically approved
Varelogianni, G., Strid, H., Oliynyk, I., Roomans, G. M. & Johannesson, M.The effect of ambroxol on chloride transport and mRNA expression of CFTR and ENaC in cystic fibrosis airway epithelial cells.
Open this publication in new window or tab >>The effect of ambroxol on chloride transport and mRNA expression of CFTR and ENaC in cystic fibrosis airway epithelial cells
Show others...
(English)Manuscript (preprint) (Other academic)
National Category
Medical and Health Sciences
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-20478 (URN)
Available from: 2011-12-05 Created: 2011-12-05 Last updated: 2017-10-17Bibliographically approved
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