Journal
BIOLOGICAL CHEMISTRY
Volume 391, Issue 11, Pages 1333-1339Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/BC.2010.133
Keywords
beta-catenin; connexin-43; lung epithelial cells; nanoparticles; stress signaling; ultrafine carbon black
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Funding
- Deutsche Forschungsgemeinschaft (DFG, Bonn, Germany) [SFB 575/B4]
- German Federal Ministry for the Environment (Bundesministerium fur Umwelt, Naturschutz und Reaktorsicherheit)
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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 beta-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.
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