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Silver nanoparticles increase connexin43‐mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen‐activated protein kinase signal pathway
Author(s) -
Qin Yu,
Han Limin,
Yang Di,
Wei Hongying,
Liu Yue,
Xu Junhui,
Autrup Herman,
Deng Furong,
Guo Xinbiao
Publication year - 2018
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3563
Subject(s) - hacat , microbiology and biotechnology , connexin , reactive oxygen species , downregulation and upregulation , protein kinase a , intracellular , kinase , chemistry , extracellular , signal transduction , mapk/erk pathway , gap junction , biology , biochemistry , in vitro , gene
Silver nanoparticles (AgNPs) are widely used in health and consumer products that routinely contact skin. However, the biological effects and possible mechanisms of AgNPs on skin remain unclear. Gap junctional intercellular communication (GJIC) plays a critical role in multicellular organisms to maintain tissue homeostasis. The aim of this study is to examine if non‐coated AgNPs affect GJIC in human keratinocytes (HaCaT cells), and to identify the possible molecular mechanisms responsible for the effects. GJIC, connexin (Cx)43 protein and mRNA expression, and the effect of siRNA‐mediated knockdown of Cx43 on GJIC were assessed. HaCaT cells exposed to non‐coated AgNPs at different doses after a 24 hour exposure. To explore further the underlying mechanism, reactive oxygen species and mitogen‐activated protein kinase pathway were evaluated after 2, 6, 12 and 24 hours. Our results revealed that non‐coated AgNP exposure at subcytotoxic doses increase GJIC partially via Cx43 upregulation. Reactive oxygen species and extracellular signal‐regulated kinase and activation of c‐Jun N‐terminal kinase were involved in the AgNP‐induced upregulation of Cx43. This study provides new insight into the potential mechanism of AgNP biological activity.