Dermatophagoides extract-treated confluent type II epithelial cells (cA549) and human lung mesenchymal cell growth

2005 ◽  
Vol 95 (4) ◽  
pp. 381-388 ◽  
Author(s):  
Anthony Capetandes ◽  
Nathanael S. Horne ◽  
Marianne Frieri
Keyword(s):  
Cell Growth ◽  
Epithelial Cells ◽  
Human Lung ◽  
Mesenchymal Cell ◽  
Type Ii

scholarly journals Keratins and protein synthesis: the plot thickens

2009 ◽  
Vol 187 (2) ◽  
pp. 157-159 ◽  
Author(s):  
Juliane C. Kellner ◽  
Pierre A. Coulombe
Keyword(s):  
Protein Synthesis ◽  
Cell Growth ◽  
Epithelial Cells ◽  
Mechanical Stress ◽  
Gene Cluster ◽  
Organelle Transport ◽  
Type Ii ◽  
Keratin Gene ◽  
Cell Biol ◽  
Keratin Proteins

In addition to protecting epithelial cells from mechanical stress, keratins regulate cytoarchitecture, cell growth, proliferation, apoptosis, and organelle transport. In this issue, Vijayaraj et al. (2009. J. Cell Biol. doi:10.1083/jcb.200906094) expand our understanding of how keratin proteins participate in the regulation of protein synthesis through their analysis of mice lacking the entire type II keratin gene cluster.

Isoflurane Regulates Atypical Type-A γ-Aminobutyric Acid Receptors in Alveolar Type II Epithelial Cells

2013 ◽  
Vol 118 (5) ◽  
pp. 1065-1075 ◽  
Author(s):  
Yun-Yan Xiang ◽  
Xuanmao Chen ◽  
Jingxin Li ◽  
Shuanglian Wang ◽  
Gil Faclier ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Gabaa Receptor ◽  
Gabaa Receptors ◽  
Human Lung ◽  
A549 Cells ◽  
Volatile Anesthetics ◽  
Aminobutyric Acid ◽  
Alveolar Type ◽  
Type Ii ◽  
Cox 2

Abstract Background: Volatile anesthetics act primarily through upregulating the activity of γ-aminobutyric acid type A (GABAA) receptors. They also exhibit antiinflammatory actions in the lung. Rodent alveolar type II (ATII) epithelial cells express GABAA receptors and the inflammatory factor cyclooxygenase-2 (COX-2). The goal of this study was to determine whether human ATII cells also express GABAA receptors and whether volatile anesthetics upregulate GABAA receptor activity, thereby reducing the expression of COX-2 in ATII cells. Methods: The expression of GABAA receptor subunits and COX-2 in ATII cells of human lung tissue and in the human ATII cell line A549 was studied with immunostaining and immunoblot analyses. Patch clamp recordings were used to study the functional and pharmacological properties of GABAA receptors in cultured A549 cells. Results: ATII cells in human lungs and cultured A549 cells expressed GABAA receptor subunits and COX-2. GABA induced currents in A549 cells, with half-maximal effective concentration of 2.5 µm. Isoflurane (0.1–250 µm) enhanced the GABA currents, which were partially inhibited by bicuculline. Treating A549 cells with muscimol or with isoflurane (250 µm) reduced the expression of COX-2, an effect that was attenuated by cotreatment with bicuculline. Conclusions: GABAA receptors expressed by human ATII cells differ pharmacologically from those in neurons, exhibiting a higher affinity for GABA and lower sensitivity to bicuculline. Clinically relevant concentrations of isoflurane increased the activity of GABAA receptors and reduced the expression of COX-2 in ATII cells. These findings reveal a novel mechanism that could contribute to the antiinflammatory effect of isoflurane in the human lung.

scholarly journals Temporal-spatial distribution of SP-B and SP-C proteins and mRNAs in developing respiratory epithelium of human lung.

1994 ◽  
Vol 42 (9) ◽  
pp. 1187-1199 ◽  
Author(s):  
A Khoor ◽  
M T Stahlman ◽  
M E Gray ◽  
J A Whitsett
Keyword(s):  
Spatial Distribution ◽  
Epithelial Cells ◽  
Human Lung ◽  
Lipid Synthesis ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Proteolytic Processing ◽  
Type Ii Cells ◽  
Type Ii ◽  
Temporal And Spatial Distribution

We determined the temporal and spatial distribution of surfactant protein B (pro-SP-B) and C (pro-SP-C) mRNAs and proteins by immunohistochemistry and in situ hybridization in fetal, neonatal, and adult human lung. Pro-SP-B and SP-B mRNA were detected in bronchi and bronchioles by 15 weeks' gestation. After 25 weeks, pro-SP-B, active SP-B peptide, and SP-B mRNA were co-localized in bronchiolo-alveolar portal cells and in Type II epithelial cells. In adult lung, pro-SP-B and SP-B mRNA were detected primarily in non-ciliated bronchiolar epithelial cells and in Type II cells in the alveolus. Pro-SP-C and SP-C mRNA were detected in cells lining terminal airways from 15 weeks' gestation and thereafter. After 25 weeks, SP-C mRNA and precursor protein were detected in epithelial cells of the bronchiolo-alveolar portals and in Type II cells, where expression increased with advancing gestational age. Distinct cellular patterns of staining for pro-SP-B compared with SP-B active peptide support the concept that its proteolytic processing or cellular routing may be influenced by cell type and/or cell differentiation. SP-B and SP-C are expressed primarily in distal conducting and terminal airway epithelium of human fetal lung well in advance of surfactant lipid synthesis or physiologic requirements to produce pulmonary surfactant at the time of birth.

Visualization of phosphatidylcholine (16:0/16:0) in type II alveolar epithelial cells in the human lung using imaging mass spectrometry

2013 ◽  
Vol 63 (4) ◽  
pp. 195-200 ◽  
Author(s):  
Nobuya Kurabe ◽  
Takahiro Hayasaka ◽  
Hisaki Igarashi ◽  
Hiroki Mori ◽  
Keigo Sekihara ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Epithelial Cells ◽  
Human Lung ◽  
Imaging Mass Spectrometry ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Toll-like receptor 2 is expressed by alveolar epithelial cells type II and macrophages in the human lung

2003 ◽  
Vol 119 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Daniel Droemann ◽  
Torsten Goldmann ◽  
Detlev Branscheid ◽  
Ryan Clark ◽  
Klaus Dalhoff ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Human Lung ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Toll Like Receptor ◽  
Alveolar Epithelial ◽  
Toll Like Receptor 2

scholarly journals Mechanism of lipopolysaccharide-mediated induction of epithelial-mesenchymal transition of alveolar type II epithelial cells in absence of other inflammatory cells

2021 ◽  
Vol 19 ◽  
pp. 205873922110144
Author(s):  
Shuai Wu ◽  
Huan Ye ◽  
TianJiao Xue ◽  
Jiali Wang
Keyword(s):  
Epithelial Cells ◽  
Pulmonary Fibrosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Cell ◽  
Expression Level ◽  
Alveolar Type ◽  
Type Ii ◽  
Gram Negative ◽  
Mesenchymal Transition ◽  
Tgf Β1

Several studies have shown that gram-negative bacilli infection can cause acute lung injury, and that consequent pulmonary fibrosis is caused when alveolar type-II epithelial cells undergo epithelial-mesenchymal transition (EMT). However, the mechanism underlying this change remains unclear. This study aimed to elucidate whether the main toxin of gram-negative bacteria, lipopolysaccharide (LPS), can induce EMT in human alveolar epithelial cells, and the underlying molecular mechanisms. Human alveolar type-II epithelial cells (A549) were used in EMT induction experiments. Cells were collected after LPS exposure, and changes in the expression levels of epithelial and mesenchymal cell markers were determined. Further, the effect of LPS exposure on the expression of Toll-like Receptor 4 (TLR4), Transforming Growth Factor-beta 1 (TGF-β1) and Smad2/3 was assessed. The expression level of a mesenchymal cell marker was also assessed after pharmacological inhibition of TLR4 and TGF-β1 prior to addition of LPS, to identify downstream pathways involved in EMT induction. Results showed that LPS exposure caused significant downregulation of epithelial marker E-cadherin, and upregulation of mesenchymal marker vimentin, together with increased expression of TGF-β1 and activation of the TGF-β1/Smad2/3 pathway. Furthermore, pretreatment with TGF-β1 and TLR4 inhibitors suppressed EMT, and treatment with the latter also reduced the expression level of TGF-β1. Overall, we conclude that LPS directly induces EMT in A549 cells through upregulation of TLR4 and activation of the TGF-β1/Smad2/3 signalling pathway. Our results suggest that LPS-mediated pulmonary fibrosis may occur in ALI patients even if the LPS-induced inflammatory response is inhibited.

Expression of a calmodulin inhibitor peptide in progenitor alveolar type II cells disrupts lung development

1996 ◽  
Vol 271 (2) ◽  
pp. L245-L250 ◽  
Author(s):  
J. Wang ◽  
B. Campos ◽  
M. A. Kaetzel ◽  
J. R. Dedman
Keyword(s):  
Cell Growth ◽  
Epithelial Cells ◽  
Lung Development ◽  
Branching Morphogenesis ◽  
Lung Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Calmodulin Inhibitor ◽  
Inhibitor Peptide ◽  
Cell Growth And Differentiation

Calmodulin (CaM) is a major intracellular Ca2+ mediator protein involved in cell growth and differentiation. To evaluate calmodulin function in lung, it was necessary to construct a gene that encodes a high-affinity calmodulin binding peptide, since chemically synthesized calmodulin inhibitors lack binding and targeting specificity. This calmodulin inhibitor peptide gene was targeted to type II epithelial cells in transgenic mice using the human surfactant protein C promoter. Neutralization of calmodulin function in progenitor type II epithelial pneumocytes alters epithelial cell growth and differentiation, which prevents branching morphogenesis of the bronchial tree. Newborn transgenic animals have undeveloped lungs. This study indicates that type II lung epithelial cells require functional CaM for proliferation and development. The targeting of specific inhibitor peptides to a single lung cell type is an approach to evaluate the role of calmodulin, the ubiquitous calcium-dependent regulator protein, in lung development and disease.

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