Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles
Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles
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DOI：
10.1515/bc.2010.133
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发表时间：
2010-11-01
影响因子：
3.7
通讯作者：
Klotza, Lars-Oliver
中科院分区：
文献类型：
--
作者：
Ale-Agha, Niloofar;Albrecht, Catrin;Klotza, Lars-Oliver
本研究旨在探讨细、超细炭黑（fC、ufC）和细、超细二氧化硅（fS、ufS）颗粒对大鼠肺上皮细胞间隙连接细胞间通讯（GJIC）的影响。在染料转移实验中，细胞暴露于亚细胞毒性剂量的ufC、fS和ufS分别导致GJIC减少63%、59%和77%。与ufC相比，fC没有显著改变GJIC。在暴露于ufC、fS或ufS的细胞中，观察到RLE细胞中主要间隙连接蛋白、连接蛋白-43 （Cx43）和β -连环蛋白亚细胞定位的变化。n -乙酰半胱氨酸抵消了GJIC的损失，并在很大程度上被表皮生长因子受体依赖信号的特异性抑制剂所阻止，这表明两种已知的纳米颗粒作用的主要介质，即活性氧和膜受体信号，在颗粒诱导的GJIC调节中起着至关重要的作用。
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.