EGF and K<sup>+</sup> channel activity control normal and cystic fibrosis bronchial epithelia repair

Trinh, Nguyen Thu Ngan; Privé, Anik; Maillé, Émilie; Noël, Jean-François; Brochiero, Emmanuelle

doi:10.1152/ajplung.90224.2008

Cited by 72 publications

(140 citation statements)

References 56 publications

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“…This suggests a negatively charged inside and a positively charged outside that can be adjusted by an active transport of Na þ ions, simple diffusion, or pumping excess ions out of the cell. K þ channels play roles in stem cell differentiation and in left-right patterning of Xenopus embryos (Morokuma et al, 2008a,b), branchial epithelia repair (Trinh et al, 2008), epithelial wound healing (Lotz et al, 2004), myoblast migration (van Lunteren et al, 2002), embryonic spinal neuron activity (Chang and Spitzer, 2009), and neuronal signaling in Xenopus embryos (Gravagna et al, 2008). We found that K þ levels do not vary within B-S-T regions, in both amputated and uncut tails.…”

Section: Developmental Dynamicsmentioning

confidence: 53%

Ion imaging during axolotl tail regeneration in vivo

Özkucur

Epperlein

Funk

2010

Developmental Dynamics

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Several studies have reported that endogenous ion currents are involved in a wide range of biological processes from single cell and tissue behavior to regeneration. Various methods are used to assess intracellular and local ion dynamics in biological systems, e.g., patch clamping and vibrating probes. Here, we introduce an approach to detect ion kinetics in vivo using a noninvasive method that can electrophysiologically characterize an entire experimental tissue region or organism. Ion-specific vital dyes have been successfully used for live imaging of intracellular ion dynamics in vitro. Here, we demonstrate that cellular pH, cell membrane potential, calcium, sodium and potassium can be monitored in vivo during tail regeneration in the axolotl (Ambystoma mexicanum) using ion-specific vital dyes. Thus, we suggest that ion-specific vital dyes can be a powerful tool to obtain electrophysiological data during crucial biological events in vivo.

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Section: Developmental Dynamicsmentioning

confidence: 53%

Ion imaging during axolotl tail regeneration in vivo

Özkucur

Epperlein

Funk

2010

Developmental Dynamics

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“…Short-circuit currents (Isc) [30][31][32] were measured through CFBE and primary airway cells [28] that had been cultured on coated permeant filters until they reached an air-liquid interface and formed a polarised epithelium with high resistance [33,34]. Measurements were performed (see supplementary material for details) on intact monolayers or through apical membranes after permeabilisation of the basolateral side with 7.5 µM amphotericin B (Sigma-Aldrich), in the presence of a symmetrical physiological solution or a chloride (Cl − ) gradient, as indicated in figure legends.…”

Section: Electrophysiologymentioning

confidence: 99%

Deleterious impact ofPseudomonas aeruginosaon cystic fibrosis transmembrane conductance regulator function and rescue in airway epithelial cells

et al. 2015

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The epithelial response to bacterial airway infection, a common feature of lung diseases such as chronic obstructive pulmonary disease and cystic fibrosis, has been extensively studied. However, its impact on cystic fibrosis transmembrane conductance regulator (CFTR) channel function is not clearly defined. Our aims were, therefore, to evaluate the effect of Pseudomonas aeruginosa on CFTR function and expression in non-cystic fibrosis airway epithelial cells, and to investigate its impact on ΔF508-CFTR rescue by the VRT-325 corrector in cystic fibrosis cells.CFTR expression/maturation was evaluated by immunoblotting and its function by short-circuit current measurements.A 24-h exposure to P. aeruginosa diffusible material (PsaDM) reduced CFTR currents as well as total and membrane protein expression of the wildtype (wt) CFTR protein in CFBE-wt cells. In CFBE-ΔF508 cells, PsaDM severely reduced CFTR maturation and current rescue induced by VRT-325. We also confirmed a deleterious impact of PsaDM on wt-CFTR currents in non-cystic fibrosis primary airway cells as well as on the rescue of ΔF508-CFTR function induced by VRT-325 in primary cystic fibrosis cells.These findings show that CFTR function could be impaired in non-cystic fibrosis patients infected by P. aeruginosa. Our data also suggest that CFTR corrector efficiency may be affected by infectious components, which should be taken into account in screening assays of correctors. @ERSpublications Exposure of airway epithelial cell to P. aeruginosa impairs CFTR function, expression and rescue by correctors http://ow.ly/IleTw

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“…It has been reported that levels of LXA 4 are reduced in CF airways (19). These observations suggest that the reduced capacity for epithelial repair described in the CF epithelium may be exacerbated or caused by low levels of LXA 4 (1,19,45).…”

mentioning

confidence: 92%

“…Repeated insults to the airway epithelium result in damage and remodeling of the airway, resulting in a decline in lung function (33,34). Epithelial repair is triggered to restore the epithelial airway architecture; however, recent research suggests that this process is impaired in CF epithelial cells (16,27,44,45).…”

mentioning

confidence: 99%

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Buchanan

McNally

Harvey

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Buchanan PJ, McNally P, Harvey BJ, Urbach V. Lipoxin A4-mediated K ATP potassium channel activation results in cystic fibrosis airway epithelial repair. Am J Physiol Lung Cell Mol Physiol 305: L193-L201, 2013. First published May 17, 2013 doi:10.1152/ajplung.00058.2013The main cause of morbidity and mortality in cystic fibrosis (CF) is progressive lung destruction as a result of persistent bacterial infection and inflammation, coupled with reduced capacity for epithelial repair. Levels of the anti-inflammatory mediator lipoxin A4 (LXA4) have been reported to be reduced in bronchoalveolar lavages of patients with CF. We investigated the ability of LXA4 to trigger epithelial repair through the initiation of proliferation and migration in non-CF (NuLi-1) and CF (CuFi-1) airway epithelia. Spontaneous repair and cell migration were significantly slower in CF epithelial cultures (CuFi-1) compared with controls (NuLi-1). LXA4 triggered an increase in migration, proliferation, and wound repair of non-CF and CF airway epithelia. These responses to LXA 4 were completely abolished by the ALX/FPR2 receptor antagonist, Boc2 and ALX/FPR2 siRNA. The KATP channel opener pinacidil mimicked the LXA4 effect on migration, proliferation, and epithelial repair, whereas the KATP channel inhibitor, glibenclamide, blocked the responses to LXA4. LXA4 did not affect potassium channel expression but significantly upregulated glibenclamide-sensitive (KATP) currents through the basolateral membrane of NuLi-1 and CuFi-1 cells. MAP kinase (ERK1/2) inhibitor, PD98059, also inhibited the LXA4-induced proliferation of NuLi-1 and CuFi-1 cells. Finally, both LXA4 and pinacidil stimulated ERK-MAP kinase phosphorylation, whereas the effect of LXA4 on ERK phosphorylation was inhibited by glibenclamide. Taken together, our results provided evidence for a role of LXA4 in triggering epithelial repair through stimulation of the ALX/FPR2 receptor, K ATP potassium channel activation, and ERK phosphorylation. This work suggests exogenous delivery of LXA4, restoring levels in patients with CF, perhaps as a potential therapeutic strategy.

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EGF and K⁺ channel activity control normal and cystic fibrosis bronchial epithelia repair

Abstract: Trinh NT, Privé A, Maillé E, Noël J, Brochiero E. EGF and K ϩ channel activity control normal and cystic fibrosis bronchial epithelia repair.

Cited by 72 publications

References 56 publications

Ion imaging during axolotl tail regeneration in vivo

Ion imaging during axolotl tail regeneration in vivo

Deleterious impact ofPseudomonas aeruginosaon cystic fibrosis transmembrane conductance regulator function and rescue in airway epithelial cells

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

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EGF and K+ channel activity control normal and cystic fibrosis bronchial epithelia repair

Abstract: Trinh NT, Privé A, Maillé E, Noël J, Brochiero E. EGF and K ϩ channel activity control normal and cystic fibrosis bronchial epithelia repair.

Cited by 72 publications

References 56 publications

Ion imaging during axolotl tail regeneration in vivo

Ion imaging during axolotl tail regeneration in vivo

Deleterious impact ofPseudomonas aeruginosaon cystic fibrosis transmembrane conductance regulator function and rescue in airway epithelial cells

Lipoxin A4-mediated KATP potassium channel activation results in cystic fibrosis airway epithelial repair

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Resources

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EGF and K⁺ channel activity control normal and cystic fibrosis bronchial epithelia repair

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair