Differential Effects Of TGF-² On Expression Of Phenotype Markers And Prepro-Endothelin-1 And Release Of Endothelin-1 In Human Alveolar Type Lung (A-549) And Bronchial (H-292) Epithelial Cells

2010 ◽  
Author(s):  
Mareille Warnken ◽  
Ahmedat S. Ahmedat ◽  
Meinolf Stöber ◽  
Ulrich Reitzenstein ◽  
Stefan M. Holtin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Type ◽  
Differential Effects ◽  
Endothelin 1 ◽  
Phenotype Markers

Connexin expression by alveolar epithelial cells is regulated by extracellular matrix

2001 ◽  
Vol 280 (2) ◽  
pp. L191-L202 ◽  
Author(s):  
Yihe Guo ◽  
Cara Martinez-Williams ◽  
Clare E. Yellowley ◽  
Henry J. Donahue ◽  
D. Eugene Rannels
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Gap Junction ◽  
Intercellular Communication ◽  
Translational Regulation ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Gap Junction Intercellular Communication ◽  
Type Ii Cell

Extracellular matrix (ECM) proteins promote attachment, spreading, and differentiation of cultured alveolar type II epithelial cells. The present studies address the hypothesis that the ECM also regulates expression and function of gap junction proteins, connexins, in this cell population. Expression of cellular fibronectin and connexin (Cx) 43 increase in parallel during early type II cell culture as Cx26 expression declines. Gap junction intercellular communication is established over the same interval. Cells plated on a preformed, type II cell-derived, fibronectin-rich ECM demonstrate accelerated formation of gap junction plaques and elevated gap junction intercellular communication. These effects are blocked by antibodies against fibronectin, which cause redistribution of Cx43 protein from the plasma membrane to the cytoplasm. Conversely, cells cultured on a laminin-rich ECM, Matrigel, express low levels of Cx43 but high levels of Cx26, reflecting both transcriptional and translational regulation. Cx26 and Cx43 thus demonstrate reciprocal regulation by ECM constituents.

In vitro time- and dose-effect response of JP-8 and S-8 jet fuel on alveolar type II epithelial cells of rats

2010 ◽  
Vol 26 (6) ◽  
pp. 367-374 ◽  
Author(s):  
Tiffany M Robb ◽  
Michael J Rogers ◽  
Suann S Woodward ◽  
Simon S Wong ◽  
Mark L Witten
Keyword(s):  
Epithelial Cells ◽  
Jet Fuel ◽  
Dose Effect ◽  
Alveolar Type ◽  
Type Ii

Carbon nanoparticle-induced lung epithelial cell proliferation is mediated by receptor-dependent Akt activation

2008 ◽  
Vol 294 (2) ◽  
pp. L358-L367 ◽  
Author(s):  
Klaus Unfried ◽  
Ulrich Sydlik ◽  
Katrin Bierhals ◽  
Alexander Weissenberg ◽  
Josef Abel
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Carbon Nanoparticles ◽  
Growth Factor Receptor ◽  
Lung Epithelial Cells ◽  
Alveolar Type ◽  
Specific Cell ◽  
Akt Inhibitor ◽  
Signaling Mechanism ◽  
Lung Epithelial

Treatment of lung epithelial cells with different kinds of nano-sized particles leads to cell proliferation. Because bigger particles fail to induce this reaction, it is suggested that the special surface properties, due to the extremely small size of these kinds of materials, is the common principle responsible for this specific cell reaction. Here the activation of the protein kinase B (Akt) signaling cascade by carbon nanoparticles was investigated with regard to its relevance for proliferation. Kinetics and dose-response experiments demonstrated that Akt is specifically activated by nanoparticulate carbon particles in rat alveolar type II epithelial cells as well as in human bronchial epithelial cells. This pathway appeared to be dependent on epidermal growth factor receptor and β1-integrins. The activation of Akt by these receptors is known to be a feature of adhesion-dependent signaling. However, intracellular proteins described in this context (focal adhesion kinase pp125FAK and integrin-linked kinase) were not activated, indicating a specific signaling mechanism. Inhibitor studies demonstrate that nanoparticle-induced proliferation is mediated by phosphoinositide 3-kinases and Akt. Moreover, overexpression of mutant Akt, as well as pretreatment with an Akt inhibitor, reduced nanoparticle-specific ERK1/2 phosphorylation, which is decisive for nanoparticle-induced proliferation. With this report, we describe the activation of a pathway by carbon nanoparticles that was so far known to be triggered by ligand receptor binding or on cell adhesion to extracellular matrix proteins.

scholarly journals EphB6 Regulates TFEB-Lysosomal Pathway and Survival of Disseminated Indolent Breast Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1079
Author(s):  
Manuela Zangrossi ◽  
Patrizia Romani ◽  
Probir Chakravarty ◽  
Colin D.H. Ratcliffe ◽  
Steven Hooper ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Lung Epithelial Cells ◽  
Late Relapse ◽  
Alveolar Type ◽  
Type I ◽  
Extrinsic Factors ◽  
Lung Epithelial

Late relapse of disseminated cancer cells is a common feature of breast and prostate tumors. Several intrinsic and extrinsic factors have been shown to affect quiescence and reawakening of disseminated dormant cancer cells (DDCCs); however, the signals and processes sustaining the survival of DDCCs in a foreign environment are still poorly understood. We have recently shown that crosstalk with lung epithelial cells promotes survival of DDCCs of estrogen receptor-positive (ER+) breast tumors. By using a lung organotypic system and in vivo dissemination assays, here we show that the TFEB-lysosomal axis is activated in DDCCs and that it is modulated by the pro-survival ephrin receptor EphB6. TFEB lysosomal direct targets are enriched in DDCCs in vivo and correlate with relapse in ER+ breast cancer patients. Direct coculture of DDCCs with alveolar type I-like lung epithelial cells and dissemination in the lung drive lysosomal accumulation and EphB6 induction. EphB6 contributes to survival, TFEB transcriptional activity, and lysosome formation in DDCCs in vitro and in vivo. Furthermore, signaling from EphB6 promotes the proliferation of surrounding lung parenchymal cells in vivo. Our data provide evidence that EphB6 is a key factor in the crosstalk between disseminated dormant cancer cells and the lung parenchyma and that the TFEB-lysosomal pathway plays an important role in the persistence of DDCCs.

Fluid transport across cultured rat alveolar epithelial cells: a novel in vitro system

2004 ◽  
Vol 287 (1) ◽  
pp. L104-L110 ◽  
Author(s):  
Xiaohui Fang ◽  
Yuanlin Song ◽  
Rachel Zemans ◽  
Jan Hirsch ◽  
Michael A. Matthay
Keyword(s):  
Epithelial Cells ◽  
Fluid Transport ◽  
Alveolar Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Morphological Evidence ◽  
Alveolar Type ◽  
Type Ii ◽  
In Vitro System ◽  
Alveolar Epithelial

Previous studies have used fluid-instilled lungs to measure net alveolar fluid transport in intact animal and human lungs. However, intact lung studies have two limitations: the contribution of different distal lung epithelial cells cannot be studied separately, and the surface area for fluid absorption can only be approximated. Therefore, we developed a method to measure net vectorial fluid transport in cultured rat alveolar type II cells using an air-liquid interface. The cells were seeded on 0.4-μm microporous inserts in a Transwell system. At 96 h, the transmembrane electrical resistance reached a peak level (1,530 ± 115 Ω·cm2) with morphological evidence of tight junctions. We measured net fluid transport by placing 150 μl of culture medium containing 0.5 μCi of 131I-albumin on the apical side of the polarized cells. Protein permeability across the cell monolayer, as measured by labeled albumin, was 1.17 ± 0.34% over 24 h. The change in concentration of 131I-albumin in the apical fluid was used to determine the net fluid transported across the monolayer over 12 and 24 h. The net basal fluid transport was 0.84 μl·cm−2·h−1. cAMP stimulation with forskolin and IBMX increased fluid transport by 96%. Amiloride inhibited both the basal and stimulated fluid transport. Ouabain inhibited basal fluid transport by 93%. The cultured cells retained alveolar type II-like features based on morphologic studies, including ultrastructural imaging. In conclusion, this novel in vitro system can be used to measure net vectorial fluid transport across cultured, polarized alveolar epithelial cells.

Sign in / Sign up

Export Citation Format

Share Document