Cx26 regulates proliferation of repairing basal airway epithelial cells

Crespin, Sophie; Bacchetta, Marc; Saab, J. Bou; Tantilipikorn, Pongsakorn; Bellec, Jessica; Dudez, Tecla; Nguyen, Tin; Kwak, Brenda R.; Lacroix, Jean‐Silvain; Huang, Sarah X.L.; Wiszniewski, Ludovic; Chanson, Marc

doi:10.1016/j.biocel.2014.02.010

Cited by 28 publications

(41 citation statements)

References 36 publications

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“…Double positive CK14/ p63-positive basal cells are rare in the airway and such cells have been associated with injury or wound-healing responses. 42 Interestingly, Oh et al 22 have shown that primary human keratinocytes transfected with ΔNp63 underwent EMT when they had depleted their normal proliferative capacity. Thus, injury-response CK14/p63-positive cells in the epithelium overlying the fibroblastic foci could be a cellular source for EMT.…”

Section: Discussionmentioning

confidence: 99%

Basal cells of the human airways acquire mesenchymal traits in idiopathic pulmonary fibrosis and in culture

Jónsdóttir

Arason

Pálsson

et al. 2015

Laboratory Investigation

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Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with high morbidity and mortality. The cellular source of the fibrotic process is currently under debate with one suggested mechanism being epithelial-to-mesenchymal transition (EMT) in the alveolar region. In this study, we show that airway epithelium overlying fibroblastic foci in IPF contains a layer of p63-positive basal cells while lacking ciliated and goblet cells. This basal epithelium shows increased expression of CK14, Vimentin and N-cadherin while retaining E-cadherin. The underlying fibroblastic foci shows both E-and N-cadherin-positive cells. To determine if p63-positive basal cells were able to undergo EMT in culture, we treated VA10, a p63-positive basal cell line, with the serum replacement UltroserG. A sub-population of treated cells acquired a mesenchymal phenotype, including an E-to N-cadherin switch. After isolation, these cells portrayed a phenotype presenting major hallmarks of EMT (loss of epithelial markers, gain of mesenchymal markers, increased migration and anchorage-independent growth). This phenotypic switch was prevented in p63 knockdown (KD) cells. In conclusion, we show that airway epithelium overlying fibroblastic foci in IPF lacks its characteristic functional identity, shows increased reactivity of basal cells and acquisition of a partial EMT phenotype. This study suggests that some p63-positive basal cells are prone to phenotypic changes and could act as EMT progenitors in IPF.

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Section: Discussionmentioning

confidence: 99%

Basal cells of the human airways acquire mesenchymal traits in idiopathic pulmonary fibrosis and in culture

Jónsdóttir

Arason

Pálsson

et al. 2015

Laboratory Investigation

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“…It has been shown that CFTR plays a critical role in this mechanism. Although it is not clear whether a defective CFTR decreases or enhances wound healing, many studies show that bronchial epithelial cells lacking CFTR are not able to reconstitute a fully differentiated epithelium [110–112]. …”

Section: Role Of Cftr In the Lungsmentioning

confidence: 99%

Role of CFTR in epithelial physiology

Saint‐Criq

Gray

2016

Cell. Mol. Life Sci.

302

291

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Salt and fluid absorption and secretion are two processes that are fundamental to epithelial function and whole body fluid homeostasis, and as such are tightly regulated in epithelial tissues. The CFTR anion channel plays a major role in regulating both secretion and absorption in a diverse range of epithelial tissues, including the airways, the GI and reproductive tracts, sweat and salivary glands. It is not surprising then that defects in CFTR function are linked to disease, including life-threatening secretory diarrhoeas, such as cholera, as well as the inherited disease, cystic fibrosis (CF), one of the most common life-limiting genetic diseases in Caucasian populations. More recently, CFTR dysfunction has also been implicated in the pathogenesis of acute pancreatitis, chronic obstructive pulmonary disease (COPD), and the hyper-responsiveness in asthma, underscoring its fundamental role in whole body health and disease. CFTR regulates many mechanisms in epithelial physiology, such as maintaining epithelial surface hydration and regulating luminal pH. Indeed, recent studies have identified luminal pH as an important arbiter of epithelial barrier function and innate defence, particularly in the airways and GI tract. In this chapter, we will illustrate the different operational roles of CFTR in epithelial function by describing its characteristics in three different tissues: the airways, the pancreas, and the sweat gland.

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“…We focused on 3 connexins (Cx26, Cx30, and Cx43) that have been implicated in acute and chronic inflammation, wound healing, and in lower airway pathology . Connexin investigations in diabetic wounds have revealed elevated levels of Cx26 and Cx43 in diabetic rats.…”

Section: Discussionmentioning

confidence: 99%