Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles
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Niloofar Ale-Agha
Abstract
The aim of this study was to investigate whether fine and ultrafine carbon black (fC and ufC), and fine and ultrafine silica (fS, ufS) particles affect gap junctional intercellular communication (GJIC) in rat lung epithelial cells. Exposure of cells to subcytotoxic doses of ufC, fS and ufS resulted in a 63%, 59% and 77% reduction of GJIC, respectively, as determined in a dye transfer assay. In contrast to ufC, fC did not significantly alter GJIC. Changes in subcellular localization of the major gap junction protein in RLE cells, connexin-43 (Cx43), and of β-catenin were observed in cells exposed to ufC, fS or ufS. The loss of GJIC was counteracted by N-acetyl cysteine and was largely prevented by specific inhibitors of epidermal growth factor receptor-dependent signaling, pointing to the crucial role of two known major mediators of nanoparticle action, namely reactive oxygen species and membrane-receptor signaling, in particle-induced modulation of GJIC.
©2010 by Walter de Gruyter Berlin New York
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- Guest Editorial
- Highlight: Xenobiotics and Cell Signaling
- Reviews
- An introduction to the molecular basics of aryl hydrocarbon receptor biology
- Mechanisms and cell signaling in alcoholic liver disease
- Superoxide anion and hydrogen peroxide-induced signaling and damage in angiotensin II and aldosterone action
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