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Chloride transport in NCL-SG3 sweat gland cells: channels involved
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2007 (English)In: Experimental and molecular pathology (Print), ISSN 0014-4800, E-ISSN 1096-0945, Vol. 83, no 1, 47-53 p.Article in journal (Refereed) Published
Abstract [en]

The aim of the study was to assess whether NCL-SG3, the only immortalized sweat gland cell line available, can be used as an in vitro model to study chloride ion transport in cultured sweat gland cells. Cl efflux was measured using the MQAE dye fluorescence technique after stimulating the cells with different agonists. A significant stimulation of chloride efflux was achieved with the calcium ionophore A23187 resulting in an efflux rate of 0.9 mM/s. Both ATP and UTP activated chloride efflux in these cells, with the ATP response being larger. IBMX and forskolin stimulation did not induce a rate of chloride efflux above the basal level. Immunocytochemistry showed no detectable CFTR in NCL-SG3 cells. This finding was confirmed with flow cytometry analysis. Niflumic acid (20 and 100 μM NFA) and 4,4′-diisothiocyanatodihydrostilbene-2,2′-disulfonic acid (H2DIDS) (100 ìM) decreased the rate of ATP-stimulated chloride efflux significantly (0.40 and 0.31 mM/s with NFA, 0.37 mM/s with H2DIDS). Gadolinium (20 ìM) had no effect on the chloride transport rate. In conclusion, the NCL-SG3 cells retain some of the aspects of human sweat gland epithelium, such as the ability to form cell–cell contacts. The CFTR protein is neither functional nor expressed in cultured NCL-SG3 sweat gland cells. Ca2+-activated chloride conductance is confirmed and the putative Ca2+-activated chloride channel (CaCC) is further characterized in term of its pharmacological sensitivity. The NCL-SG3 sweat gland cell line can be used to investigate the characteristics of the CaCC and to identify the channel.

Place, publisher, year, edition, pages
2007. Vol. 83, no 1, 47-53 p.
Keyword [en]
Biological Markers, Calcium/metabolism, Cell Line, Chloride Channels/*metabolism, Chlorides/*metabolism, Epithelial Cells/metabolism, Humans, Immunohistochemistry, Ion Channel Gating, Ion Transport, Microscopy; Electron; Transmission, Sweat Glands/*metabolism/ultrastructure
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-17161DOI: 10.1016/j.yexmp.2007.02.003ISI: 000247716800008PubMedID: 17383636OAI: oai:DiVA.org:uu-17161DiVA: diva2:44932
Available from: 2008-06-17 Created: 2008-06-17 Last updated: 2017-12-08Bibliographically approved
In thesis
1. Functional Aspects of Epithelia in Cystic Fibrosis and Asthma
Open this publication in new window or tab >>Functional Aspects of Epithelia in Cystic Fibrosis and Asthma
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP activated chloride channel in the apical membrane of epithelial cells, is defective in patients with cystic fibrosis (CF). Research efforts are focused on chloride channel function in order to find a cure for the disease.

Genistein increased chloride transport in normal and delF508-CFTR cultured airway epithelial cells without cAMP stimulation. Prior pretreatment with phenylbutyrate did not affect the rate of the genistein-stimulated chloride efflux in these cells.

S-nitrosoglutathione is an endogenous bronchodilator, present in decreased amounts in the lungs of CF patients. We studied the effect of GSNO on chloride (Cl-) transport in primary nasal epithelial cells from CF patients homozygous for the delF508-CFTR mutation, as well as in two CF cell lines, using a fluorescent Cl- indicator and X-ray microanalysis. GSNO increased chloride efflux in the CF cell lines and in primary nasal epithelial cells from CF patients. This effect was partly mediated by CFTR. If the cells were exposed to GSNO in the presence of L-cysteine, Cl- transport was enhanced after 5 min, but not after 4 h. GSNO may be a candidate for pharmacological treatment of CF patients.

Chloride transport properties of cultured NCL-SG3 sweat gland cells were investigated. The CFTR protein was neither functional nor expressed in these cells. Ca2+-activated chloride conductance was confirmed and the putative Ca2+-activated chloride channel (CaCC) was further characterized in term of its pharmacological sensitivity.

Corticosteroids, the primary treatment for asthma, cause necrosis/apoptosis of airway epithelial cells. It was investigated whether a newer generation of drugs used in asthma, leukotriene receptor antagonists, had similar effects. Both montelukast and dexamethasone, but not beclomethasone or budesonide induced apoptosis/necrosis in superficial airway epithelial cells. Montelukast and corticosteroids also caused decreased expression of intercellular adhesion molecule -1 (ICAM-1) in epithelial but not endothelial cells.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2008. 91 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 361
Keyword
Cell biology, cystic fibrosis, CFTR, chloride transport, airway epithelium, sweat gland, asthma, corticosteroids, montelukast, Cellbiologi
Identifiers
urn:nbn:se:uu:diva-8905 (URN)978-91-554-7224-5 (ISBN)
Public defence
2008-06-05, B7:113a, BMC, Husargatan 3, Uppsala, 13:15
Opponent
Supervisors
Available from: 2008-05-15 Created: 2008-05-15 Last updated: 2013-09-20Bibliographically approved

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Roomans, Godfried M.

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