Chronic exposure of lung alveolar epithelial type II cells to tobacco-specific carcinogen NNK results in malignant transformation: A new in vitro lung carcinogenesis model

2012 ◽  
Vol 53 (5) ◽  
pp. 392-402 ◽  
Author(s):  
Gregory Mennecier ◽  
Luciana N. Torres ◽  
Bruno Cogliati ◽  
Daniel S. Sanches ◽  
Claudia M. Mori ◽  
...  
Keyword(s):  
Malignant Transformation ◽  
Chronic Exposure ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Carcinogenesis ◽  
Alveolar Epithelial

Disparate cytokine regulation of ICAM-1 in rat alveolar epithelial cells and pulmonary endothelial cells in vitro

1995 ◽  
Vol 269 (1) ◽  
pp. L127-L135 ◽  
Author(s):  
W. W. Barton ◽  
S. Wilcoxen ◽  
P. J. Christensen ◽  
R. Paine
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Alveolar Epithelial Cells ◽  
Normal Lung ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Morphologic Damage of Rat Alveolar Epithelial Type II Cells Induced by Bile Acids Could Be Ameliorated by Farnesoid X Receptor Inhibitor Z-Guggulsterone In Vitro

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jieqin Wang ◽  
Yaowei Huang ◽  
Xusheng Hou ◽  
Wenyu Wu ◽  
Lei Nie ◽  
...  
Keyword(s):  
Bile Acids ◽  
Farnesoid X Receptor ◽  
Ultrastructural Changes ◽  
Respiratory Disorder ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Transmission Electron ◽  
High Level

Objective. To determine whether bile acids (BAs) affect respiratory functions through the farnesoid X receptor (FXR) expressed in the lungs and to explore the possible mechanisms of BAs-induced respiratory disorder.Methods. Primary cultured alveolar epithelial type II cells (AECIIs) of rat were treated with different concentrations of chenodeoxycholic acid (CDCA) in the presence or absence of FXR inhibitor Z-guggulsterone (GS). Then, expression of FXR in nuclei of AECIIs was assessed by immunofluorescence microscopy. And ultrastructural changes of the cells were observed under transmission electron microscope and analyzed by Image-Pro Plus software.Results. Morphologic damage of AECIIs was exhibited in high BAs group in vitro, with high-level expression of FXR, while FXR inhibitor GS could attenuate the cytotoxicity of BAs to AECIIs.Conclusions. FXR expression was related to the morphologic damage of AECIIs induced by BAs, thus influencing respiratory functions.

Injury of rat pulmonary alveolar epithelial cells by H2O2: dependence on phenotype and catalase

1991 ◽  
Vol 260 (4) ◽  
pp. L318-L325 ◽  
Author(s):  
R. H. Simon ◽  
J. A. Edwards ◽  
M. M. Reza ◽  
R. G. Kunkel
Keyword(s):  
Epithelial Cells ◽  
Catalase Activity ◽  
Lung Diseases ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

In a variety of inflammatory lung diseases, type I alveolar epithelial cells are more likely to be injured than are type II cells. Because oxidants have been implicated as a cause of injury in various inflammatory lung diseases, we evaluated the effects of differentiation on alveolar epithelial cell susceptibility to H2O2-induced injury. With the use of isolated rat type II cells in culture, we found that the cytotoxic effect of H2O2 increased between days 2 and 7, when type II cells are known to lose their distinctive type II properties and assume a more type I-like appearance. We previously reported that type II cells utilized both intracellular catalase and glutathione-dependent reactions to protect against H2O2. We therefore examined whether alterations in either of these protective mechanisms were responsible for the differentiation-dependent changes in sensitivity to H2O2. We found that catalase activity within alveolar epithelial cells decreased between 2 and 7 days in culture, whereas no changes were detected in glutathione-dependent systems. We then used a histochemical technique that detects catalase activity and found that type II cells within rat lungs possessed numerous catalase-containing peroxisomes, whereas very few were detected in type I cells. These findings demonstrate that as type II cells assume a type I-like phenotype, they become more susceptible to H2O2-induced injury. This increased susceptibility is associated with reductions in intracellular catalase activity, both in vitro and in vivo.

Hepatocyte growth factor stimulates DNA synthesis in alveolar epithelial type II cells in vitro.

1995 ◽  
Vol 12 (2) ◽  
pp. 171-180 ◽  
Author(s):  
M Shiratori ◽  
G Michalopoulos ◽  
H Shinozuka ◽  
G Singh ◽  
H Ogasawara ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Dna Synthesis ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Hepatocyte Growth

In vitro expansion of endogenous human alveolar epithelial type II cells in fibroblast-free spheroid culture

2019 ◽  
Vol 515 (4) ◽  
pp. 579-585 ◽  
Author(s):  
Kazushige Shiraishi ◽  
Takuya Nakajima ◽  
Shigeyuki Shichino ◽  
Shungo Deshimaru ◽  
Kouji Matsushima ◽  
...  
Keyword(s):  
Type Ii Cells ◽  
Type Ii ◽  
Spheroid Culture ◽  
Alveolar Epithelial ◽  
In Vitro Expansion

scholarly journals Mechanical distension modulates pulmonary alveolar epithelial phenotypic expression in vitro

1998 ◽  
Vol 274 (2) ◽  
pp. L196-L202 ◽  
Author(s):  
Jorge A. Gutierrez ◽  
Robert F. Gonzalez ◽  
Leland G. Dobbs
Keyword(s):  
Phenotypic Expression ◽  
Alveolar Type ◽  
Transcriptional Level ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Alveolar Epithelial ◽  
Mrna Content

The pulmonary alveolar epithelium is composed of two distinct types of cells, type I and type II cells, both of which are critical for normal lung function. On the basis of experiments of both nature and in vivo studies, it has been hypothesized that expression of the type I or type II phenotype is influenced by mechanical factors. We have investigated the effects of mechanical distension on the expression of specific markers for the type I and type II cell phenotypes in cultured alveolar type II cells. Rat alveolar type II cells were tonically mechanically distended in culture. Cells were analyzed for a marker for the type I phenotype (rTI40, an integral membrane protein specific for type I cells) and for markers for the type II phenotype [surfactant protein (SP) A, SP-B, and SP-C] as well as for glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Mechanical distension caused a 68 ± 25% ( n = 3) increase in mRNA content of rTI40 relative to undistended controls. In contrast, mechanical distension resulted in a decrease in mRNA content of SP-B to 35 ± 19% ( n = 3) and of SP-C to 20 ± 6.7% ( n = 3) of undistended controls. There was no effect on mRNA content of SP-A or GAPDH. The differences in mRNA content of SP-B and SP-C were found to be primarily due to changes at the transcriptional level by nuclear run-on assays. The effects on rTI40 appear to be due to posttranscriptional events. These data show that mechanical distension influences alveolar epithelial phenotypic expression in vitro, at least in part, at the transcriptional level.

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