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dc.contributor.authorTorr, Een_US
dc.contributor.authorHeath, Men_US
dc.contributor.authorMee, Men_US
dc.contributor.authorShaw, Den_US
dc.contributor.authorSharp, TVen_US
dc.contributor.authorSayers, Ien_US
dc.date.accessioned2017-02-27T10:33:33Z
dc.date.available2016-06-07en_US
dc.date.issued2016-08en_US
dc.date.submitted2017-02-24T07:58:55.020Z
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/19543
dc.description.abstractThe airway epithelium is altered in respiratory disease and is thought to contribute to disease etiology. A caveat to disease research is that the technique of isolation of bronchial epithelial cells from patients is invasive and cells have a limited lifespan. The aim of this study was to extensively characterize the plasticity of primary human bronchial epithelial cells that have been engineered to delay cell senescence including the ability of these cells to differentiate. Cells were engineered to express BMI-1 or hTERT using viral vector systems. Cells were characterized at passage (p) early (p5), mid (p10), and late (p15) stage for: BMI-1, p16, and CK14 protein expression, viability and the ability to differentiate at air-liquid interface (ALI), using a range of techniques including immunohistochemistry (IHC), immunofluorescence (IF), transepithelial electrical resistance (TEER), scanning electron microscopy (SEM), MUC5AC and beta tubulin (BTUB) staining. BMI-1-expressing cells maintained elevated levels of the BMI-1 protein and the epithelial marker CK14 and showed a suppression of p16. BMI-1-expressing cells had a viability advantage, differentiated at ALI, and had a normal karyotype. In contrast, hTERT-expressing cells had a reduced viability, showed limited differentiation, and had an abnormal karyotype. We therefore provide extensive characterization of the plasticity of BMI-1 expressing cells in the context of the ALI model. These cells retain properties of wild-type cells and may be useful to characterize respiratory disease mechanisms in vitro over sustained periods.en_US
dc.description.sponsorshipAsthma UK Grant 10/006.en_US
dc.languageengen_US
dc.language.isoenen_US
dc.relation.ispartofPhysiol Repen_US
dc.rightsCC BY
dc.subjectBMI‐1en_US
dc.subjectbronchial epithelial cellsen_US
dc.subjectlifespanen_US
dc.subjectplasticityen_US
dc.subjectAdulten_US
dc.subjectBronchien_US
dc.subjectCell Differentiationen_US
dc.subjectCell Plasticityen_US
dc.subjectCellular Senescenceen_US
dc.subjectEpithelial Cellsen_US
dc.subjectGenes, p16en_US
dc.subjectGenetic Engineeringen_US
dc.subjectHumansen_US
dc.subjectIn Vitro Techniquesen_US
dc.subjectKaryotypeen_US
dc.subjectLentivirusen_US
dc.subjectMaleen_US
dc.subjectMiddle Ageden_US
dc.subjectPeptide Fragmentsen_US
dc.subjectPolycomb Repressive Complex 1en_US
dc.subjectRetroviridaeen_US
dc.subjectTelomeraseen_US
dc.titleExpression of polycomb protein BMI-1 maintains the plasticity of basal bronchial epithelial cells.en_US
dc.typeArticle
dc.identifier.doi10.14814/phy2.12847en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/27558999en_US
pubs.issue16en_US
pubs.notesNot knownen_US
pubs.publication-statusPublisheden_US
pubs.volume4en_US
dcterms.dateAccepted2016-06-07en_US


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