Lipopolysaccharide changes the subcellular distribution of aquaporin 5 and increases plasma membrane water permeability in mouse lung epithelial cells

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.

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Nitric oxide decreases cell surface expression of aquaporin-5 and membrane water permeability in lung epithelial cells

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2007.01.026 ◽

2007 ◽

Vol 354 (2) ◽

pp. 579-584 ◽

Cited By ~ 11

Author(s):

Kazufumi Nagai ◽

Megumi Watanabe ◽

Mayumi Seto ◽

Akinori Hisatsune ◽

Takeshi Miyata ◽

...

Keyword(s):

Nitric Oxide ◽

Epithelial Cells ◽

Cell Surface ◽

Water Permeability ◽

Surface Expression ◽

Lung Epithelial Cells ◽

Cell Surface Expression ◽

Aquaporin 5 ◽

Lung Epithelial

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

Journal of Biological Chemistry ◽

10.1074/jbc.m100322200 ◽

2001 ◽

Vol 276 (22) ◽

pp. 18657-18664 ◽

Cited By ~ 95

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

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Effect of Slit/Robo signaling on regeneration in lung emphysema

Experimental & Molecular Medicine ◽

10.1038/s12276-021-00633-8 ◽

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.

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