Long-term stimulation of alveolar epithelial cells by β-adrenergic agonists: increased Na+ transport and modulation of cell growth?

2003 ◽  
Vol 285 (4) ◽  
pp. L798-L801 ◽  
Author(s):  
Yves Berthiaume
Keyword(s):  
Cell Growth ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Adrenergic Agonists ◽  
Na Transport ◽  
Alveolar Epithelial ◽  
Stimulation Of

Cl-channel activation is necessary for stimulation of Na transport in adult alveolar epithelial cells

2000 ◽  
Vol 278 (2) ◽  
pp. L239-L244 ◽  
Author(s):  
Scott M. O'Grady ◽  
Xinpo Jiang ◽  
David H. Ingbar
Keyword(s):  
Epithelial Cells ◽  
Adrenergic Receptor ◽  
Apical Membrane ◽  
Receptor Activation ◽  
Alveolar Epithelial Cells ◽  
Na Channels ◽  
Channel Activation ◽  
Alveolar Epithelial ◽  
Cl Channel ◽  
Stimulation Of

In this review, we discuss evidence that supports the hypothesis that adrenergic stimulation of transepithelial Na absorption across the alveolar epithelium occurs indirectly by activation of apical Cl channels, resulting in hyperpolarization and an increased driving force for Na uptake through amiloride-sensitive Na channels. This hypothesis differs from the prevailing idea that adrenergic-receptor activation increases the open probability of Na channels, leading to an increase in apical membrane Na permeability and an increase in Na and fluid uptake from the alveolar space. We review results from cultured alveolar epithelial cell monolayer experiments that show increases in apical membrane Cl conductance in the absence of any change in Na conductance after stimulation by selective β-adrenergic-receptor agonists. We also discuss possible reasons for differences in Na-channel regulation in cells grown in monolayer culture compared with that in dissociated alveolar epithelial cells. Finally, we describe some preliminary in vivo data that suggest a role for Cl-channel activation in the process of amiloride-sensitive alveolar fluid absorption.

Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A

1994 ◽  
Vol 266 (2) ◽  
pp. L148-L155 ◽  
Author(s):  
H. Blau ◽  
S. Riklis ◽  
V. Kravtsov ◽  
M. Kalina
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Long Term Culture ◽  
Alveolar Epithelial ◽  
Gm Csf

Cultured alveolar type II cells and pulmonary epithelial (PE) cells in long-term culture were found to secrete colony-stimulating factors (CSF) into the medium in similar fashion to alveolar macrophages. CSF activity was determined by using the in vitro assay for myeloid progenitor cells [colony-forming units in culture (CFU-C)]. Both lipopolisaccharide (LPS) and interleukin-1 alpha (IL-1 alpha) were found to upregulate the secretion 6.5- to 8-fold from alveolar type II cells and macrophages. However, no stimulatory effect of these factors was observed in PE cells that release CSF into the medium constitutively, possibly due to the conditions of long-term culture. The CSF activity was partially neutralized (70% inhibition) by antibodies against murine granulocyte/macrophage (GM)-CSF and IL-3, thus indicating the presence of both GM-CSF and IL-3-like factors in the CSF. However, the presence of other cytokines in the CSF is highly probable. Surfactant-associated protein A (SP-A), which is known to play a central role in surfactant homeostasis and function, was also found to upregulate secretion of CSF (at concentrations of 0.1-5 micrograms/ml) from alveolar type II cells and macrophages. Control cells such as rat peritoneal macrophages, alveolar fibroblasts, and 3T3/NIH cell line could not be elicited by SP-A to release CSF. The results are discussed in relation to the possible participation of the alveolar epithelial cells in various intercellular signaling networks. Our studies suggest that alveolar type II cells and SP-A may play an important regulatory role in the modulation of immune and inflammatory effector cells within the alveolar space.

scholarly journals Mechanisms of EGF-induced stimulation of sodium reabsorption by alveolar epithelial cells

1998 ◽  
Vol 275 (1) ◽  
pp. C82-C92 ◽  
Author(s):  
Spencer I. Danto ◽  
Zea Borok ◽  
Xiao-Ling Zhang ◽  
Melissa Z. Lopez ◽  
Paryus Patel ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Cell Labeling ◽  
Northern Analysis ◽  
Sodium Reabsorption ◽  
Alveolar Epithelial ◽  
Subunit Mrna ◽  
Epidermal Growth ◽  
Stimulation Of

We investigated the effects of epidermal growth factor (EGF) on active Na+ absorption by alveolar epithelium. Rat alveolar epithelial cells (AEC) were isolated and cultivated in serum-free medium on tissue culture-treated polycarbonate filters. mRNA for rat epithelial Na+ channel (rENaC) α-, β-, and γ-subunits and Na+ pump α1- and β1-subunits were detected in day 4 monolayers by Northern analysis and were unchanged in abundance in day 5 monolayers in the absence of EGF. Monolayers cultivated in the presence of EGF (20 ng/ml) for 24 h from day 4 to day 5 showed an increase in both α1 and β1Na+ pump subunit mRNA but no increase in rENaC subunit mRNA. EGF-treated monolayers showed parallel increases in Na+ pump α1- and β1-subunit protein by immunoblot relative to untreated monolayers. Fixed AEC monolayers demonstrated predominantly membrane-associated immunofluorescent labeling with anti-Na+ pump α1- and β1-subunit antibodies, with increased intensity of cell labeling for both subunits seen at 24 h following exposure to EGF. These changes in Na+ pump mRNA and protein preceded a delayed (>12 h) increase in short-current circuit (measure of active transepithelial Na+transport) across monolayers treated with EGF compared with untreated monolayers. We conclude that EGF increases active Na+ resorption across AEC monolayers primarily via direct effects on Na+ pump subunit mRNA expression and protein synthesis, leading to increased numbers of functional Na+ pumps in the basolateral membranes.

Adrenergic stimulation of Na+transport across alveolar epithelial cells involves activation of apical Cl−channels

1998 ◽  
Vol 275 (6) ◽  
pp. C1610-C1620 ◽  
Author(s):  
Xinpo Jiang ◽  
David H. Ingbar ◽  
Scott M. O’Grady
Keyword(s):  
Epithelial Cells ◽  
Short Circuit ◽  
Methanesulfonic Acid ◽  
Reversal Potential ◽  
Short Circuit Current ◽  
Alveolar Epithelial Cells ◽  
Sprague Dawley ◽  
Adrenergic Stimulation ◽  
Alveolar Epithelial ◽  
Stimulation Of

Alveolar epithelial cells were isolated from adult Sprague-Dawley rats and grown to confluence on membrane filters. Most of the basal short-circuit current ( I sc; 60%) was inhibited by amiloride (IC50 0.96 μM) or benzamil (IC50 0.5 μM). Basolateral addition of terbutaline (2 μM) produced a rapid decrease in I sc, followed by a slow recovery back to its initial amplitude. When Cl− was replaced with methanesulfonic acid, the basal I sc was reduced and the response to terbutaline was inhibited. In permeabilized monolayer experiments, both terbutaline and amiloride produced sustained decreases in current. The current-voltage relationship of the terbutaline-sensitive current had a reversal potential of −28 mV. Increasing Cl− concentration in the basolateral solution shifted the reversal potential to more depolarized voltages. These results were consistent with the existence of a terbutaline-activated Cl− conductance in the apical membrane. Terbutaline did not increase the amiloride-sensitive Na+ conductance. We conclude that β-adrenergic stimulation of adult alveolar epithelial cells results in an increase in apical Cl− permeability and that amiloride-sensitive Na+ channels are not directly affected by this stimulation.

Evidence for active Na+ transport by cultured monolayers of pulmonary alveolar epithelial cells

1983 ◽  
Vol 245 (1) ◽  
pp. C78-C83 ◽  
Author(s):  
B. E. Goodman ◽  
R. S. Fleischer ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Active Transport ◽  
Alveolar Epithelial Cells ◽  
Metabolic Inhibitors ◽  
Normal Lung ◽  
Type Ii ◽  
Na Transport ◽  
Alveolar Epithelial ◽  
Cl Transport ◽  
Transport Inhibitors

Primary cultured type II alveolar epithelial cells grown to confluence on nonporous surfaces form many small fluid-filled hemicysts or domes. These domes are generally thought to result from active transport of solutes from the medium above the cell monolayer to the substratum, with water following passively. We have investigated the characteristics of active transport by primary cultured monolayers of type II alveolar epithelial cells from rat lungs. Changes in dome density were measured after exposure to metabolic inhibitors, Na+ or Cl- transport inhibitors, and low-Na+ or low-Cl- culture media. Metabolic and Na+ transport inhibitors, and low-Na+ medium, lead to disappearance of domes, whereas Cl- transport inhibitors and low-Cl- medium seem to have no effect on dome density. These results suggest the presence of a Na+-dependent active transepithelial transport process across the monolayer, which is responsible for the formation of domes. This finding implies that absorption of fluid by mammalian alveolar epithelium in vivo may be important in the maintenance of normal lung fluid balance.

Design of biomimetic substrates for long-term maintenance of alveolar epithelial cells

2018 ◽  
Vol 6 (2) ◽  
pp. 292-303 ◽  
Author(s):  
James C. H. Poon ◽  
Zhongfa Liao ◽  
Takaya Suzuki ◽  
Miranda M. Carleton ◽  
John P. Soleas ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Diseases ◽  
Alveolar Epithelial Cells ◽  
Biological Mechanisms ◽  
Alveolar Epithelial ◽  
Epithelial Culture ◽  
Culture Models ◽  
Term Maintenance

There is a need to establish in vitro lung alveolar epithelial culture models to better understand the fundamental biological mechanisms that drive lung diseases.

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