scholarly journals 670: F508del and G542X sheep models exhibit a severe cystic fibrosis phenotype, and their tracheal epithelial cells respond to human therapeutics in vitro

2021 ◽  
Vol 20 ◽  
pp. S317-S318
Author(s):  
I. Viotti Perisse ◽  
Z. Fan ◽  
Y. Liu ◽  
S. Leir ◽  
A. Van Wettere ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

scholarly journals In Vitro Radiation-induced Effects on Rat Tracheal Epithelial Cells

2002 ◽  
Vol 43 (1) ◽  
pp. 27-27 ◽  
Author(s):  
CAROLE KUGEL ◽  
ISABELLE BAILLY ◽  
FRANÇOISE TOURDES ◽  
JEAN-LUC PONCY
Keyword(s):  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Radiation Induced ◽  
Tracheal Epithelial

CFTR gene transfer corrects defective glycoconjugate secretion in human CF epithelial tracheal cells

1995 ◽  
Vol 269 (6) ◽  
pp. L855-L864 ◽  
Author(s):  
M. Mergey ◽  
M. Lemnaouar ◽  
D. Veissiere ◽  
M. Perricaudet ◽  
D. C. Gruenert ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Protein Kinase ◽  
Gene Transfer ◽  
Epithelial Cells ◽  
De Novo ◽  
Tracheal Epithelial Cells ◽  
Normal Human ◽  
Cftr Protein ◽  
Tracheal Epithelial ◽  
And Control

We demonstrate that in immortalized normal human tracheal epithelial cells (NT-1 and 56FHTE8o-) 14C-labeled glycoconjugate secretion may be regulated independently by agonists of the protein kinase A (PKA) and protein kinase C (PKC) signaling pathways. In contrast, in immortalized cystic fibrosis (CF) human tracheal epithelial cells (CFT-1 and CFT-2), regulation is defective for agonists specific for the PKA but not for the PKC pathway. To characterize the involvement of the cystic fibrosis transmembrane conductance regulator (CFTR) in regulated glycoconjugate secretion, we examined the effect of adenovirus-mediated gene transfer of CFTR to CF and control cells. Forty-eight hours after infection, at a multiplicity of infection of 50 plaque-forming units per cell, high levels of CFTR mRNA were detected by reverse transcription-polymerase chain reaction, and de novo synthesis of CFTR protein was demonstrated by immunoblotting. Gene transfer to CF cells restored defective adenosine 3',5'-cyclic monophosphate (cAMP)-dependent secretion not only of chloride but also of glycoconjugates. Taken together, these results argue for a role for CFTR in cAMP-mediated glycoconjugate secretion.

scholarly journals In Vitro Radiation-induced Effects on Rat Tracheal Epithelial Cells

2002 ◽  
Vol 43 (1) ◽  
pp. 35-35 ◽  
Author(s):  
JEAN-LUC PONCY ◽  
CAROLE KUGEL ◽  
FRANÇOISE TOURDES ◽  
ISABELLE BAILLY
Keyword(s):  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Radiation Induced ◽  
Tracheal Epithelial

scholarly journals Recombinant CTFR detection in CF tracheal epithelial cells following in vitro liposomeme-mediated gene transfer

IUBMB Life ◽  
1997 ◽  
Vol 42 (4) ◽  
pp. 723-729
Author(s):  
Alessia Colosimo ◽  
Stefania Scarpino ◽  
Federica Sangiuolo ◽  
Sabrina Di Sario ◽  
Giuseppe Mossa ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Modulation of Ca2+ influx by a mediator released from human tracheal epithelial cells exposed to ozone in vitro

1995 ◽  
Vol 268 (4) ◽  
pp. L558-L564 ◽  
Author(s):  
Q. S. Qu ◽  
L. C. Chen
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Health Effects ◽  
Cellular Function ◽  
Vital Role ◽  
Tracheal Epithelial Cells ◽  
Cell Lysate ◽  
Tracheal Epithelial ◽  
Normal Cellular Function

Intracellular free Ca2+ ([Ca2+]i) plays a vital role both in maintaining normal cellular function and in cell killing. Few studies have been published regarding its role in ozone (O3)-induced health effects. This study investigated the effect and mechanism of O3 exposure on [Ca2+]i in human tracheal epithelial (HTE) cells. HTE cells grown on Costar Transwell inserts with a liquid-gas interface were exposed to 0, 0.05, 0.1, 0.2 and 0.4 ppm O3 at 37 degrees C for 1 h. After exposure, [Ca2+]i was measured using the fluorescent dye Fluo 3. O3 at 0.4 ppm produced a significant increase in [Ca2+]i, and the increases in [Ca2+]i were blocked by verapamil and 8-(diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). These results suggest that the O3-induced [Ca2+]i elevation may involve both Ca2+ release from internal stores and Ca2+ influx across the plasma membrane. Furthermore, both buffer and cell lysate of HTE cells exposed to 0.4 ppm O3 caused a rapid increase in [Ca2+]i of THP-1 human phagocytic monocytes, but the buffer and lysate from air exposed cells did not. These results suggest that O3 exposure causes HTE cells to release a diffusible mediator from the empty Ca(2+)-storing organelle and may be responsible for the sustained and persistent [Ca2+]i elevation in HTE cells exposed to 0.4 ppm O3.

Activation of PtdIns(4,5)P2-sensitive phospholipase C in rabbit tracheal epithelial cells

1994 ◽  
Vol 266 (2) ◽  
pp. C397-C405 ◽  
Author(s):  
C. M. Liedtke
Keyword(s):  
Epithelial Cells ◽  
Phospholipase C ◽  
Pertussis Toxin ◽  
Inositol Phosphates ◽  
Inositol Trisphosphate ◽  
Isolated Cells ◽  
Tracheal Epithelial Cells ◽  
Adrenergic Antagonist ◽  
Tracheal Epithelial

A role for phospholipase C hydrolysis of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] as a mechanism of alpha 2-adrenergic signal transduction in rabbit tracheal epithelial cells (tracheocytes) was investigated in isolated cells grown in in vitro culture and prelabeled with myo-[3H]inositol (3 microCi/ml) for 72 h. Breakdown of polyphosphoinositides was measured by using thin-layer chromatography to detect phosphatidylinositol, phosphatidylinositol 4-phosphate [PtdIns(4)P], and PtdIns(4,5)P2. Inositol phosphates were separated by ion-exchange column chromatography. The endogenous catecholamine l-epinephrine and alpha 2-adrenergic agonists clonidine and 1-(2,6-dichlorobenzylideneamino)guanidine (guanabenz) produced a rapid transient accumulation of inositol trisphosphate and inositol 4,5-bisphosphate and breakdown of [PtdIns(4)P] and PtdIns(4,5)P2. The alpha 2-adrenergic effects were not blocked by the beta-adrenergic antagonist DL-propranolol or by the alpha 1-adrenergic antagonists prazosin and methylurapidil but were inhibited by pertussis toxin and blocked by yohimbine, an alpha 2-adrenergic antagonist. The 50% effective concentration for guanabenz-stimulated inositol trisphosphate generation was right shifted from 0.3 to 0.9 microM by yohimbine. The results provide the first demonstration of alpha 2A-adrenergic activation of pertussis toxin-sensitive PtdIns(4,5)P2-dependent phospholipase C in mammalian tracheocytes. The findings are consistent with previous observations on alpha 2A-adrenergic-mediated activation of NaCl cotransport in these cells.

H2O2 induces apoptosis in bovine tracheal epithelial cells in vitro

Life Sciences ◽  
1999 ◽  
Vol 64 (26) ◽  
pp. 2489-2496 ◽  
Author(s):  
Yuri Nakajima ◽  
Kazutetsu Aoshiba ◽  
Shuji Yasui ◽  
Atsushi Nagai
Keyword(s):  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Tracheal matrices, obtained by a detergent-enzymatic method, support in vitro the adhesion of chondrocytes and tracheal epithelial cells

2005 ◽  
Vol 18 (6) ◽  
pp. 727-734 ◽  
Author(s):  
Maria Teresa Conconi ◽  
Paolo De Coppi ◽  
Rosa Di Liddo ◽  
Simonetta Vigolo ◽  
Giovanni Franco Zanon ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Enzymatic Method ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial
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