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dc.contributor.authorS. Crespinen_US
dc.contributor.authorM. Bacchettaen_US
dc.contributor.authorJ. Bou Saaben_US
dc.contributor.authorP. Tantilipikornen_US
dc.contributor.authorJ. Bellecen_US
dc.contributor.authorT. Dudezen_US
dc.contributor.authorT. H. Nguyenen_US
dc.contributor.authorB. R. Kwaken_US
dc.contributor.authorJ. S. Lacroixen_US
dc.contributor.authorS. Huangen_US
dc.contributor.authorL. Wiszniewskien_US
dc.contributor.authorM. Chansonen_US
dc.contributor.otherHopitaux universitaires de Geneveen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherCentre Hospitalier Universitaire de Nantesen_US
dc.contributor.otherUniversite de Geneveen_US
dc.contributor.otherEpithelix Sàrlen_US
dc.date.accessioned2018-11-09T02:00:08Z-
dc.date.available2018-11-09T02:00:08Z-
dc.date.issued2014-01-01en_US
dc.identifier.citationInternational Journal of Biochemistry and Cell Biology. Vol.52, (2014), 152-160en_US
dc.identifier.issn18785875en_US
dc.identifier.issn13572725en_US
dc.identifier.other2-s2.0-84901634896en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84901634896&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/33478-
dc.description.abstractThe recovery of an intact epithelium following injury is critical for restoration of lung homeostasis, a process that may be altered in cystic fibrosis (CF). In response to injury, progenitor cells in the undamaged areas migrate, proliferate and re-differentiate to regenerate an intact airway epithelium. The mechanisms regulating this regenerative response are, however, not well understood. In a model of circular wound injury of well-differentiated human airway epithelial cell (HAEC) cultures, we identified the gap junction protein Cx26 as an important regulator of cell proliferation. We report that induction of Cx26 in repairing HAECs is associated with cell proliferation. We also show that Cx26 is expressed in a population of CK14-positive basal-like cells. Cx26 silencing in immortalized cell lines using siRNA and in primary HAECs using lentiviral-transduced shRNA enhanced Ki67-labeling index and Ki67 mRNA, indicating that Cx26 acts a negative regulator of HAEC proliferation. Cx26 silencing also markedly decreased the transcription of KLF4 in immortalized HAECs. We further show that CF HAECs exhibited deregulated expression of KLF4, Ki67 and Cx26 as well enhanced rate of wound closure in the early response to injury. These results point to an altered repair process of CF HAECs characterized by rapid but desynchronized initiation of HAEC activation and proliferation. This article is part of a Directed Issue entitled: Cystic fibrosis: From o-mics to cell biology, physiology, and therapeutic advances. © 2014 Elsevier Ltd.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84901634896&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleCx26 regulates proliferation of repairing basal airway epithelial cellsen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1016/j.biocel.2014.02.010en_US
Appears in Collections:Scopus 2011-2015

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