Effects of vitamin A on proliferation of human distal airway epithelial cells in culture

1994 ◽  
Vol 424 (5) ◽  
Author(s):  
T. Shibagaki ◽  
T. Ogata ◽  
H. Kitamura ◽  
Y. Inayama ◽  
M. Kanisawa
Keyword(s):  
Epithelial Cells ◽  
Vitamin A ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cells In Culture ◽  
Distal Airway

scholarly journals Regulation of Thioredoxin Gene Expression by Vitamin A in Human Airway Epithelial Cells

2002 ◽  
Vol 26 (5) ◽  
pp. 627-635 ◽  
Author(s):  
Wen-Hsing Chang ◽  
Sekhar P.-M. Reddy ◽  
Yuan-Pu Peter Di ◽  
Ken Yoneda ◽  
Richart Harper ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Vitamin A ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Ambroxol Inhibits Na+ Absorption by Canine Airway Epithelial Cells in Culture

1991 ◽  
Vol 43 (12) ◽  
pp. 841-843 ◽  
Author(s):  
Jun Tamaoki ◽  
Atsushi Chiyotani ◽  
Fumiko Yamauchi ◽  
Satomi Takeuchi ◽  
Takao Takizawa
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cells In Culture

Stimulation of Cl Secretion by Lactoferrin across Canine Airway Epithelial Cells in Culture

Respiration ◽  
1992 ◽  
Vol 59 (4) ◽  
pp. 189-192 ◽  
Author(s):  
A. Chiyotani ◽  
J. Tamaoki ◽  
F. Yamauchi ◽  
S. Takeuchi ◽  
T. Kanemura ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cl Secretion ◽  
Cells In Culture ◽  
Stimulation Of

Respiratory epithelial cells regulate lung inflammation in response to inhaled endotoxin

2004 ◽  
Vol 287 (1) ◽  
pp. L143-L152 ◽  
Author(s):  
Shawn J. Skerrett ◽  
H. Denny Liggitt ◽  
Adeline M. Hajjar ◽  
Robert K. Ernst ◽  
Samuel I. Miller ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Transgenic Mice ◽  
Lung Inflammation ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Respiratory Epithelial Cells ◽  
Distal Airway ◽  
Tnf Α ◽  
Respiratory Epithelial

To determine the role of respiratory epithelial cells in the inflammatory response to inhaled endotoxin, we selectively inhibited NF-κB activation in the respiratory epithelium using a mutant IκB-α construct that functioned as a dominant negative inhibitor of NF-κB translocation (dnIκB-α). We developed two lines of transgenic mice in which expression of dnIκB-α was targeted to the distal airway epithelium using the human surfactant apoprotein C promoter. Transgene expression was localized to the epithelium of the terminal bronchioles and alveoli. After inhalation of LPS, nuclear translocation of NF-κB was evident in bronchiolar epithelium of nontransgenic but not of transgenic mice. This defect was associated with impaired neutrophilic lung inflammation 4 h after LPS challenge and diminished levels of TNF-α, IL-1β, macrophage inflammatory protein-2, and KC in lung homogenates. Expression of TNF-α within bronchiolar epithelial cells and of VCAM-1 within peribronchiolar endothelial cells was reduced in transgenic animals. Thus targeted inhibition of NF-κB activation in distal airway epithelial cells impaired the inflammatory response to inhaled LPS. These data provide causal evidence that distal airway epithelial cells and the signals they transduce play a physiological role in lung inflammation in vivo.

scholarly journals Expression of intermediate-conductance, Ca2+-activated K+ channel (KCNN4) in H441 human distal airway epithelial cells

2006 ◽  
Vol 291 (5) ◽  
pp. L957-L965 ◽  
Author(s):  
S. M. Wilson ◽  
S. G. Brown ◽  
N. McTavish ◽  
R. P. McNeill ◽  
E. M. Husband ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Membrane Conductance ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Channel Blockers ◽  
Resting Cells ◽  
Airway Epithelial ◽  
Distal Airway

Electrophysiological studies of H441 human distal airway epithelial cells showed that thapsigargin caused a Ca2+-dependent increase in membrane conductance ( GTot) and hyperpolarization of membrane potential ( Vm). These effects reflected a rapid rise in cellular K+ conductance ( GK) and a slow fall in amiloride-sensitive Na+ conductance ( GNa). The increase in GTot was antagonized by Ba2+, a nonselective K+ channel blocker, and abolished by clotrimazole, a KCNN4 inhibitor, but unaffected by other selective K+ channel blockers. Moreover, 1-ethyl-2-benzimidazolinone (1-EBIO), which is known to activate KCNN4, increased GK with no effect on GNa. RT-PCR-based analyses confirmed expression of mRNA encoding KCNN4 and suggested that two related K+ channels (KCNN1 and KCNMA1) were absent. Subsequent studies showed that 1-EBIO stimulates Na+ transport in polarized monolayers without affecting intracellular Ca2+ concentration ([Ca2+]i), suggesting that the activity of KCNN4 might influence the rate of Na+ absorption by contributing to GK. Transient expression of KCNN4 cloned from H441 cells conferred a Ca2+- and 1-EBIO-sensitive K+ conductance on Chinese hamster ovary cells, but this channel was inactive when [Ca2+]i was <0.2 μM. Subsequent studies of amiloride-treated H441 cells showed that clotrimazole had no effect on Vm despite clear depolarizations in response to increased extracellular K+ concentration ([K+]o). These findings thus indicate that KCNN4 does not contribute to Vm in unstimulated cells. The present data thus establish that H441 cells express KCNN4 and highlight the importance of GK to the control of Na+ absorption, but, because KCNN4 is quiescent in resting cells, this channel cannot contribute to resting GK or influence basal Na+ absorption.

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