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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred

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Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles

Niloofar Ale-Agha1 / Catrin Albrecht1 / Lars-Oliver Klotz1, a

1Leibniz-Institut für umweltmedizinische Forschung (IUF), Auf'm Hennekamp 50, D-40225 Düsseldorf, Germany

aPresent address: University of Alberta, Faculty of Pharmacy and Pharmaceutical Sciences, 3126 Dentistry/Pharmacy Centre, Edmonton, Alberta T6G 2N8, Canada.

Corresponding author

Citation Information: Biological Chemistry. Volume 391, Issue 11, Pages 1333–1339, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: 10.1515/bc.2010.133, September 2010

Publication History

Published Online:


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.

Keywords: β-catenin; connexin-43; lung epithelial cells; nanoparticles; stress signaling; ultrafine carbon black

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