Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model?
It has been reported recently that the cystic fibrosis transmembrane conductance regulator (CFTR) besides transcellular chloride transport, also controls the paracellular permeability of bronchial epithelium. The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellul...
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| creator | Molenda, Natalia Urbanova, Katarina Weiser, Nelly Kusche-Vihrog, Kristina Günzel, Dorothee Schillers, Hermann |
| description | It has been reported recently that the cystic fibrosis transmembrane conductance regulator (CFTR) besides transcellular chloride transport, also controls the paracellular permeability of bronchial epithelium. The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellular permeability of cell monolayers. To answer this question we used a CFBE41o- cell line transfected with wtCFTR or mutant F508del-CFTR and compered them with parental line and healthy 16HBE14o- cells. Transepithelial electrical resistance (TER) and paracellular fluorescein flux were measured under control and CFTR-stimulating conditions. CFTR stimulation significant decreased TER in 16HBE14o- and also in CFBE41o- cells transfected with wtCFTR. In contrast, TER increased upon stimulation in CFBE41o- cells and CFBE41o- cells transfected with F508del-CFTR. Under non-stimulated conditions, all four cell lines had similar paracellular fluorescein flux. Stimulation increased only the paracellular permeability of the 16HBE14o- cell monolayers. We observed that 16HBE14o- cells were significantly smaller and showed a different structure of cell-cell contacts than CFBE41o- and its overexpressing clones. Consequently, 16HBE14o- cells have about 80% more cell-cell contacts through which electrical current and solutes can leak. Also tight junction protein composition is different in 'healthy' 16HBE14o- cells compared to 'cystic fibrosis' CFBE41o- cells. We found that claudin-3 expression was considerably stronger in 16HBE14o- cells than in the three CFBE41o- cell clones and thus independent of the presence of functional CFTR. Together, CFBE41o- cell line transfection with wtCFTR modifies transcellular conductance, but not the paracellular permeability. We conclude that CFTR overexpression is not sufficient to fully reconstitute transport in CF bronchial epithelium. Hence, it is not recommended to use those cell lines to study CFTR-dependent epithelial transport. |
| doi_str_mv | 10.1371/journal.pone.0100621 |
| format | Article |
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The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellular permeability of cell monolayers. To answer this question we used a CFBE41o- cell line transfected with wtCFTR or mutant F508del-CFTR and compered them with parental line and healthy 16HBE14o- cells. Transepithelial electrical resistance (TER) and paracellular fluorescein flux were measured under control and CFTR-stimulating conditions. CFTR stimulation significant decreased TER in 16HBE14o- and also in CFBE41o- cells transfected with wtCFTR. In contrast, TER increased upon stimulation in CFBE41o- cells and CFBE41o- cells transfected with F508del-CFTR. Under non-stimulated conditions, all four cell lines had similar paracellular fluorescein flux. Stimulation increased only the paracellular permeability of the 16HBE14o- cell monolayers. We observed that 16HBE14o- cells were significantly smaller and showed a different structure of cell-cell contacts than CFBE41o- and its overexpressing clones. Consequently, 16HBE14o- cells have about 80% more cell-cell contacts through which electrical current and solutes can leak. Also tight junction protein composition is different in 'healthy' 16HBE14o- cells compared to 'cystic fibrosis' CFBE41o- cells. We found that claudin-3 expression was considerably stronger in 16HBE14o- cells than in the three CFBE41o- cell clones and thus independent of the presence of functional CFTR. Together, CFBE41o- cell line transfection with wtCFTR modifies transcellular conductance, but not the paracellular permeability. We conclude that CFTR overexpression is not sufficient to fully reconstitute transport in CF bronchial epithelium. Hence, it is not recommended to use those cell lines to study CFTR-dependent epithelial transport.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0100621</identifier><identifier>PMID: 24945658</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biological Transport ; Biology and Life Sciences ; Biotechnology ; Bronchi - metabolism ; Bronchi - pathology ; Cell culture ; Cell Line ; Cell lines ; Chloride transport ; Chlorides ; Claudin-3 - genetics ; Claudin-3 - metabolism ; Conductance ; Cystic fibrosis ; Cystic Fibrosis - genetics ; Cystic Fibrosis - metabolism ; Cystic Fibrosis - pathology ; Cystic Fibrosis Transmembrane Conductance Regulator - genetics ; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism ; Electric contacts ; Electric Impedance ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelium ; Fluorescein ; Fluorescein - metabolism ; Gene Expression ; Humans ; Medicine and Health Sciences ; Models, Biological ; Monolayers ; Monomolecular films ; Morphology ; Mutation ; Permeability ; Physiology ; Protein composition ; Proteins ; Resistance ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; Rodents ; Signal Transduction ; Solutes ; Stimulation ; Tight Junctions - metabolism ; Tight Junctions - pathology ; Transfection ; Transport</subject><ispartof>PloS one, 2014-06, Vol.9 (6), p.e100621-e100621</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Molenda et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Molenda et al 2014 Molenda et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-21fc9e312a1c24d626e25b6687dca173fe61f472f04c42a0ef4e9fa10d97657a3</citedby><cites>FETCH-LOGICAL-c692t-21fc9e312a1c24d626e25b6687dca173fe61f472f04c42a0ef4e9fa10d97657a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063962/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063962/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24945658$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ahmad, Shama</contributor><creatorcontrib>Molenda, Natalia</creatorcontrib><creatorcontrib>Urbanova, Katarina</creatorcontrib><creatorcontrib>Weiser, Nelly</creatorcontrib><creatorcontrib>Kusche-Vihrog, Kristina</creatorcontrib><creatorcontrib>Günzel, Dorothee</creatorcontrib><creatorcontrib>Schillers, Hermann</creatorcontrib><title>Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model?</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>It has been reported recently that the cystic fibrosis transmembrane conductance regulator (CFTR) besides transcellular chloride transport, also controls the paracellular permeability of bronchial epithelium. The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellular permeability of cell monolayers. To answer this question we used a CFBE41o- cell line transfected with wtCFTR or mutant F508del-CFTR and compered them with parental line and healthy 16HBE14o- cells. Transepithelial electrical resistance (TER) and paracellular fluorescein flux were measured under control and CFTR-stimulating conditions. CFTR stimulation significant decreased TER in 16HBE14o- and also in CFBE41o- cells transfected with wtCFTR. In contrast, TER increased upon stimulation in CFBE41o- cells and CFBE41o- cells transfected with F508del-CFTR. Under non-stimulated conditions, all four cell lines had similar paracellular fluorescein flux. Stimulation increased only the paracellular permeability of the 16HBE14o- cell monolayers. We observed that 16HBE14o- cells were significantly smaller and showed a different structure of cell-cell contacts than CFBE41o- and its overexpressing clones. Consequently, 16HBE14o- cells have about 80% more cell-cell contacts through which electrical current and solutes can leak. Also tight junction protein composition is different in 'healthy' 16HBE14o- cells compared to 'cystic fibrosis' CFBE41o- cells. We found that claudin-3 expression was considerably stronger in 16HBE14o- cells than in the three CFBE41o- cell clones and thus independent of the presence of functional CFTR. Together, CFBE41o- cell line transfection with wtCFTR modifies transcellular conductance, but not the paracellular permeability. We conclude that CFTR overexpression is not sufficient to fully reconstitute transport in CF bronchial epithelium. Hence, it is not recommended to use those cell lines to study CFTR-dependent epithelial transport.</description><subject>Biological Transport</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Bronchi - metabolism</subject><subject>Bronchi - pathology</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Chloride transport</subject><subject>Chlorides</subject><subject>Claudin-3 - genetics</subject><subject>Claudin-3 - metabolism</subject><subject>Conductance</subject><subject>Cystic fibrosis</subject><subject>Cystic Fibrosis - genetics</subject><subject>Cystic Fibrosis - metabolism</subject><subject>Cystic Fibrosis - pathology</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - metabolism</subject><subject>Electric contacts</subject><subject>Electric Impedance</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelium</subject><subject>Fluorescein</subject><subject>Fluorescein - metabolism</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Medicine and Health Sciences</subject><subject>Models, Biological</subject><subject>Monolayers</subject><subject>Monomolecular films</subject><subject>Morphology</subject><subject>Mutation</subject><subject>Permeability</subject><subject>Physiology</subject><subject>Protein composition</subject><subject>Proteins</subject><subject>Resistance</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Solutes</subject><subject>Stimulation</subject><subject>Tight Junctions - metabolism</subject><subject>Tight Junctions - pathology</subject><subject>Transfection</subject><subject>Transport</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9tu1DAQhiMEoqXwBggsISG42MWnOMkNqKo4VEIq4nRrzTrjjStvHOyk0LfH6W6rLuoFyoUt-5t_PH9miuIpo0smKvbmPEyxB78cQo9LyihVnN0rDlkj-EJxKu7f2h8Uj1I6p7QUtVIPiwMuG1mqsj4sLr5ABIPeTx4iGSP0aQhxJGMXw7TuSIfgx-6SQN8Sc5lGZ4h1qxiSSyQvvekceIKDGzv083bWIt71mBaLNpDfSDq4QAJkiGHASDahRf_ucfHAgk_4ZLceFT8-vP9-8mnx-ezj6cnx54VRDR8XnFnToGAcmOGyVVwhL1dK1VVrgFXComJWVtxSaSQHilZiY4HRtqlUWYE4Kp5vdQcfkt5ZljQrRb5nXPBMnG6JNsC5HqLbQLzUAZy-OghxrSHmsj1qAKOsgLqqZStx1UBpaduyyqxKKsHIrPV2l21abbA12GdD_Z7o_k3vOr0OF1pSJRo1P-bVTiCGXxOmUW9cmh2FHsN09e5GVoKWc64X_6B3V7ej1pALcL0NOa-ZRfWxZDUTNW-aTC3voPLX4saZ3F_W5fO9gNd7AZkZ8c-4hiklffrt6_-zZz_32Ze32G3vpeCn0YU-7YNyC5rciimivTGZUT2Px7Ubeh4PvRuPHPbs9g-6CbqeB_EXLa0MFQ</recordid><startdate>20140619</startdate><enddate>20140619</enddate><creator>Molenda, Natalia</creator><creator>Urbanova, Katarina</creator><creator>Weiser, Nelly</creator><creator>Kusche-Vihrog, Kristina</creator><creator>Günzel, Dorothee</creator><creator>Schillers, Hermann</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140619</creationdate><title>Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model?</title><author>Molenda, Natalia ; Urbanova, Katarina ; Weiser, Nelly ; Kusche-Vihrog, Kristina ; Günzel, Dorothee ; Schillers, Hermann</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-21fc9e312a1c24d626e25b6687dca173fe61f472f04c42a0ef4e9fa10d97657a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Biological Transport</topic><topic>Biology and Life Sciences</topic><topic>Biotechnology</topic><topic>Bronchi - metabolism</topic><topic>Bronchi - pathology</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Cell lines</topic><topic>Chloride transport</topic><topic>Chlorides</topic><topic>Claudin-3 - genetics</topic><topic>Claudin-3 - metabolism</topic><topic>Conductance</topic><topic>Cystic fibrosis</topic><topic>Cystic Fibrosis - genetics</topic><topic>Cystic Fibrosis - metabolism</topic><topic>Cystic Fibrosis - pathology</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator - metabolism</topic><topic>Electric contacts</topic><topic>Electric Impedance</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelium</topic><topic>Fluorescein</topic><topic>Fluorescein - metabolism</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Medicine and Health Sciences</topic><topic>Models, Biological</topic><topic>Monolayers</topic><topic>Monomolecular films</topic><topic>Morphology</topic><topic>Mutation</topic><topic>Permeability</topic><topic>Physiology</topic><topic>Protein composition</topic><topic>Proteins</topic><topic>Resistance</topic><topic>Respiratory Mucosa - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Molenda, Natalia</au><au>Urbanova, Katarina</au><au>Weiser, Nelly</au><au>Kusche-Vihrog, Kristina</au><au>Günzel, Dorothee</au><au>Schillers, Hermann</au><au>Ahmad, Shama</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model?</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-06-19</date><risdate>2014</risdate><volume>9</volume><issue>6</issue><spage>e100621</spage><epage>e100621</epage><pages>e100621-e100621</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>It has been reported recently that the cystic fibrosis transmembrane conductance regulator (CFTR) besides transcellular chloride transport, also controls the paracellular permeability of bronchial epithelium. The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellular permeability of cell monolayers. To answer this question we used a CFBE41o- cell line transfected with wtCFTR or mutant F508del-CFTR and compered them with parental line and healthy 16HBE14o- cells. Transepithelial electrical resistance (TER) and paracellular fluorescein flux were measured under control and CFTR-stimulating conditions. CFTR stimulation significant decreased TER in 16HBE14o- and also in CFBE41o- cells transfected with wtCFTR. In contrast, TER increased upon stimulation in CFBE41o- cells and CFBE41o- cells transfected with F508del-CFTR. Under non-stimulated conditions, all four cell lines had similar paracellular fluorescein flux. Stimulation increased only the paracellular permeability of the 16HBE14o- cell monolayers. We observed that 16HBE14o- cells were significantly smaller and showed a different structure of cell-cell contacts than CFBE41o- and its overexpressing clones. Consequently, 16HBE14o- cells have about 80% more cell-cell contacts through which electrical current and solutes can leak. Also tight junction protein composition is different in 'healthy' 16HBE14o- cells compared to 'cystic fibrosis' CFBE41o- cells. We found that claudin-3 expression was considerably stronger in 16HBE14o- cells than in the three CFBE41o- cell clones and thus independent of the presence of functional CFTR. Together, CFBE41o- cell line transfection with wtCFTR modifies transcellular conductance, but not the paracellular permeability. We conclude that CFTR overexpression is not sufficient to fully reconstitute transport in CF bronchial epithelium. Hence, it is not recommended to use those cell lines to study CFTR-dependent epithelial transport.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24945658</pmid><doi>10.1371/journal.pone.0100621</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1537651232 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Biological Transport Biology and Life Sciences Biotechnology Bronchi - metabolism Bronchi - pathology Cell culture Cell Line Cell lines Chloride transport Chlorides Claudin-3 - genetics Claudin-3 - metabolism Conductance Cystic fibrosis Cystic Fibrosis - genetics Cystic Fibrosis - metabolism Cystic Fibrosis - pathology Cystic Fibrosis Transmembrane Conductance Regulator - genetics Cystic Fibrosis Transmembrane Conductance Regulator - metabolism Electric contacts Electric Impedance Epithelial cells Epithelial Cells - metabolism Epithelial Cells - pathology Epithelium Fluorescein Fluorescein - metabolism Gene Expression Humans Medicine and Health Sciences Models, Biological Monolayers Monomolecular films Morphology Mutation Permeability Physiology Protein composition Proteins Resistance Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Rodents Signal Transduction Solutes Stimulation Tight Junctions - metabolism Tight Junctions - pathology Transfection Transport |
| title | Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model? |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T02%3A54%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Paracellular%20transport%20through%20healthy%20and%20cystic%20fibrosis%20bronchial%20epithelial%20cell%20lines--do%20we%20have%20a%20proper%20model?&rft.jtitle=PloS%20one&rft.au=Molenda,%20Natalia&rft.date=2014-06-19&rft.volume=9&rft.issue=6&rft.spage=e100621&rft.epage=e100621&rft.pages=e100621-e100621&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0100621&rft_dat=%3Cgale_plos_%3EA418138299%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1537651232&rft_id=info:pmid/24945658&rft_galeid=A418138299&rft_doaj_id=oai_doaj_org_article_aac6f3a8784d4eb9a5f0dd17cb504ac4&rfr_iscdi=true |