scholarly journals Oxygen‐evoked Na + transport in rat fetal distal lung epithelial cells

2001 ◽  
Vol 532 (1) ◽  
pp. 105-113 ◽  
Author(s):  
D. L. Baines ◽  
S. J. Ramminger ◽  
A. Collett ◽  
J. J. E. Haddad ◽  
O. G. Best ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Na Transport ◽  
Lung Epithelial ◽  
Distal Lung

scholarly journals Hormonal modulation of Na + transport in rat fetal distal lung epithelial cells

2002 ◽  
Vol 544 (2) ◽  
pp. 567-577 ◽  
Author(s):  
S. J. Ramminger ◽  
S. K. Inglis ◽  
R. E. Olver ◽  
S. M. Wilson
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Na Transport ◽  
Lung Epithelial ◽  
Hormonal Modulation ◽  
Distal Lung

Inhibition of amiloride-sensitive sodium-channel activity in distal lung epithelial cells by nitric oxide

1998 ◽  
Vol 274 (3) ◽  
pp. L378-L387 ◽  
Author(s):  
Jin Wen Ding ◽  
John Dickie ◽  
Hugh O’Brodovich ◽  
Yutaka Shintani ◽  
Bijan Rafii ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Cell Function ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Lung Epithelial Cells ◽  
Flufenamic Acid ◽  
Activated Macrophages ◽  
Lung Epithelial ◽  
Distal Lung

Distal lung epithelial cells (DLECs) play an active role in fluid clearance from the alveolus by virtue of their ability to actively transport Na+ from the alveolus to the interstitial space. The present study evaluated the ability of activated macrophages to modulate the bioelectric properties of DLECs. Low numbers of lipopolysaccharide (LPS)-treated macrophages were able to significantly reduce amiloride-sensitive short-circuit current ( I sc) without affecting total I sc or monolayer resistance. This was associated with a rise in the flufenamic acid-sensitive component of the I sc. The effect was reversed by the addition of N-monomethyl-l-arginine to the medium, implying a role for nitric oxide. We hypothesized that macrophages exerted their effect by expressing inducible nitric oxide synthase (iNOS) in DLECs. The products of LPS-treated macrophages increased the levels of iNOS protein and mRNA transcripts in DLECs as well as causing a rise in iNOS activity. Immunofluorescence microscopy of LPS-stimulated macrophage-DLEC cocultures with anti-nitrotyrosine antibodies provided evidence for the generation of peroxynitrite in macrophages but not in DLECs. These data indicate that activated macrophages in the lung may contribute to impaired resolution of acute respiratory distress syndrome and suggest a novel mechanism whereby nitric oxide might alter cell function by altering its ion-transporting phenotype.

Evidence for apical sodium channels in frog lung epithelial cells

1989 ◽  
Vol 256 (4) ◽  
pp. C764-C771 ◽  
Author(s):  
H. Fischer ◽  
W. Van Driessche ◽  
W. Clauss
Keyword(s):  
Epithelial Cells ◽  
Short Circuit ◽  
Lung Epithelial Cells ◽  
Power Density Spectrum ◽  
Fluctuation Analysis ◽  
Na Transport ◽  
Density Spectrum ◽  
Isolated Lung ◽  
Lung Epithelial ◽  
Single Channel Currents

To reveal the mechanism of Na+ transport across Xenopus lung epithelium, we recorded short-circuit current (Isc), transepithelial resistance (Rt), and current noise spectra while the isolated lung tissues were mounted in an Ussing-type chamber. Mean values of Isc and Rt obtained while the tissue was bilaterally incubated with NaCl-Ringer solution were Isc = 11.57 +/- 1.19 microA.cm-2 and Rt = 0.82 +/- 0.07 k omega.cm2. Amiloride added to the mucosal (apical) side depressed Isc by 61 to 99%. Ouabain abolished Isc totally when added to the basolateral compartment. Adenosine 3',5'-cyclic monophosphate (cAMP), epinephrine, and a variety of other compounds did not alter Isc significantly. Transepithelial depolarization with serosal KCl solution reduced Isc to 6.22 +/- 1.37 microA.cm-2. Amiloride-sensitive current and the kinetics of amiloride interaction were not significantly affected by depolarization. Fluctuation analysis of Isc in the presence of amiloride revealed a Lorentzian component in the power density spectrum indicating apical Na+ channels. Assuming pseudo-first order kinetics, we calculated single channel currents (iNa) and channel density (M): iNa = 0.29 +/- 0.04 pA and M = 0.24 +/- 0.04 micron 2. Our results show that the route for Na+ transport through lung epithelial cells follows the classical Koefoed-Johnson-Ussing model for tight epithelia.

scholarly journals Mechanotransduction via TRPV4 regulates inflammation and differentiation in fetal mouse distal lung epithelial cells

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Pritha S. Nayak ◽  
Yulian Wang ◽  
Tanbir Najrana ◽  
Lauren M. Priolo ◽  
Mayra Rios ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Fetal Mouse ◽  
Lung Epithelial ◽  
Distal Lung

H2O2 mediates O2 toxicity in cultured fetal rat distal lung epithelial cells

1999 ◽  
Vol 26 (11-12) ◽  
pp. 1357-1368 ◽  
Author(s):  
Xiaoping Luo ◽  
Neil A Christie ◽  
Michael A McLaughlin ◽  
Rose Belcastro ◽  
Larisa Sedlackova ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Fetal Rat ◽  
Lung Epithelial ◽  
Distal Lung

Long-term terbutaline exposure stimulates α1-Na+-K+-ATPase expression at posttranscriptional level in rat fetal distal lung epithelial cells

2010 ◽  
Vol 298 (1) ◽  
pp. L96-L104 ◽  
Author(s):  
Muhammad S. Rahman ◽  
Shephali Gandhi ◽  
Gail Otulakowski ◽  
Wenming Duan ◽  
Aparna Sarangapani ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Atpase Activity ◽  
Apical Membrane ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Lung Epithelial Cells ◽  
Intracellular Camp ◽  
Adult Type ◽  
Lung Epithelial ◽  
Distal Lung

Transepithelial Na+ transport through epithelial Na+ channels (ENaC) on the apical membrane and Na+-K+-ATPase activity on the basolateral membrane of distal lung epithelial cells are critical for alveolar fluid clearance. Acute exposure to β-adrenergic agonists stimulates lung fluid clearance by increasing Na+ transport. We investigated the effects of chronic exposure to the β2-adrenergic agonist terbutaline on the transepithelial Na+ transport in rat fetal distal lung epithelia (FDLE). FDLE monolayers exposed to 10−4 M terbutaline for 48 h had significantly increased propanolol-blockable transepithelial total and amiloride-sensitive short-circuit current ( Isc); however, when these chronically exposed monolayers were acutely exposed to additional β-agonists and intracellular cAMP upregulators, there was no further increase in Isc. Monolayers exposed to terbutaline for >48 h had Isc similar to control cells. Ouabain-sensitive Na+-K+-ATPase activity was increased in 48-h terbutaline-exposed FDLE whose apical membranes were permeabilized with nystatin. In contrast, terbutaline did not increase amiloride-sensitive apical membrane Isc in FDLE whose basolateral membranes were permeabilized with nystatin. Terbutaline treatment did not affect α-, β-, or γ-ENaC mRNA or α-ENaC protein steady-state levels, but increased total cellular levels and rate of synthesis of α1-Na+-K+-ATPase protein in FDLE in the absence of any change in α1-Na+-K+-ATPase mRNA. Total cellular β1-Na+-K+-ATPase mRNA and protein levels were not affected by terbutaline. These data suggest that FDLE have different responses from adult type II epithelial cells when chronically exposed to terbutaline, and their increased transepithelial Na+ transport occurs via a posttranscriptional increase in α1-Na+-K+-ATPase expression.

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