scholarly journals Ezrin Regulates Ca2+ Ionophore-Induced Plasma Membrane Translocation of Aquaporin-5

2021 ◽  
Vol 22 (24) ◽  
pp. 13505
Author(s):  
Shin-ichi Muroi ◽  
Yoichiro Isohama
Keyword(s):  
Plasma Membrane ◽  
Membrane Trafficking ◽  
Apical Membrane ◽  
State Level ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Aquaporin 5 ◽  
Family Protein ◽  
Lung Epithelial ◽  
Dependent Pathway

Aquaporin-5 (AQP5) is selectively expressed in the apical membrane of exocrine glands, such as salivary, sweat, and submucosal airway glands, and plays important roles in maintaining their secretory functions. Because AQP5 is not regulated by gating, localization on the plasma membrane is important for its water-permeable function. Ezrin is an ezrin–radixin–moesin family protein that serves as a crosslinker between the plasma membrane and actin cytoskeleton network. It plays important roles in translocation of various membrane proteins to mediate vesicle trafficking to the plasma membrane. In this study, we examined the effects of ezrin inhibition on membrane trafficking of AQP5. Ezrin inhibition selectively suppressed an ionomycin-induced increase in AQP5 translocation to the plasma membrane of mouse lung epithelial cells (MLE-12) without affecting the steady-state level of plasma membrane AQP5. Taken together, our data suggest that AQP5 translocates to the plasma membrane through at least two pathways and that ezrin is selectively involved in a stimulation-dependent pathway.

scholarly journals Tumor Necrosis Factor-α Inhibits Aquaporin 5 Expression in Mouse Lung Epithelial Cells

2001 ◽  
Vol 276 (22) ◽  
pp. 18657-18664 ◽  
Author(s):  
Jennifer E. Towne ◽  
Carissa M. Krane ◽  
Cindy J. Bachurski ◽  
Anil G. Menon
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Aquaporin 5 ◽  
Lung Epithelial ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Effect of Slit/Robo signaling on regeneration in lung emphysema

2021 ◽  
Author(s):  
Jin-Soo Park ◽  
RyeonJin Cho ◽  
Eun-Young Kang ◽  
Yeon-Mok Oh
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Chronic Obstructive ◽  
Irreversible Damage ◽  
Lung Epithelial ◽  
And Migration ◽  
Proliferation And Migration

AbstractEmphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.

scholarly journals Ex vivo model of non‑small cell lung cancer using mouse lung epithelial cells

2017 ◽  
Author(s):  
Taku Sato ◽  
Mami Morita ◽  
Ryota Tanaka ◽  
Yui Inoue ◽  
Miyuki Nomura ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Small Cell Lung Cancer ◽  
Ex Vivo ◽  
Small Cell ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Small Cell Lung ◽  
Ex Vivo Model ◽  
Lung Epithelial

scholarly journals 33 Sodium 4-phenylbutyrate induces IL-8 expression in CF lung epithelial cells through an ERK1/2-dependent pathway

2006 ◽  
Vol 5 ◽  
pp. S8
Author(s):  
E. Boncoeur ◽  
T. Roque ◽  
O. Tabary ◽  
E. Bonvin ◽  
A. Clement ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Dependent Pathway

scholarly journals Selection of rhinovirus 1A variants adapted for growth in mouse lung epithelial cells

Virology ◽  
2011 ◽  
Vol 420 (2) ◽  
pp. 82-88 ◽  
Author(s):  
Angela L. Rasmussen ◽  
Vincent R. Racaniello
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Selection Of

Hypoxia results in an HIF-1-dependent induction of brain-specific aldolase C in lung epithelial cells

2006 ◽  
Vol 291 (5) ◽  
pp. L950-L956 ◽  
Author(s):  
Jyh-Chang Jean ◽  
Celeste B. Rich ◽  
Martin Joyce-Brady
Keyword(s):  
Hypoxia Inducible Factor ◽  
Fetal Lung ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Developmentally Regulated ◽  
Specific Expression ◽  
Aldolase C ◽  
Expression Studies ◽  
Lung Epithelial ◽  
Responsive Element

Aldolase C (EC 4.1.2.13 ) is a brain-specific aldolase isoform and a putative target of the transcription factor hypoxia-inducible factor (HIF)-1. We identified aldolase C as a candidate hypoxia-regulated gene in mouse lung epithelial (MLE) cells using differential display. We show that the message accumulates in a robust fashion when MLE cells are exposed to 1% oxygen and is inversely related to oxygen content. Induction in hypoxia is dependent on protein synthesis. We localized a hypoxia-responsive element (HRE) in the aldolase C promoter using a series of deletion and heterologous expression studies. The HRE overlaps with a region of the proximal aldolase C promoter that is also related to its brain-specific expression. The HRE contains an Arnt (HIF-1β) and an HIF-1α site. We show that induction in hypoxia is dependent on the HIF-1 site and that HIF-1α protein is present, by gel-shift assay, within nuclear complexes of MLE cells in hypoxia. Aldolase C mRNA expression is developmentally regulated in the fetal lung, rapidly downregulated in the newborn lung at birth, and inducible in the adult lung when exposed to hypoxia. This pattern of regulation is not seen in the brain. This preservation of this HRE in the promoters of four other species suggests that aldolase C may function as a stress-response gene.

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