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 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

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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