Transient suppression of gap junctional intercellular communication after exposure to 100-nanosecond pulsed electric fields
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
27439151
DOI
10.1016/j.bioelechem.2016.07.003
PII: S1567-5394(16)30087-1
Knihovny.cz E-zdroje
- Klíčová slova
- Actin, Connexin 43, Cx43, GJIC, MAP kinase, nsPEF,
- MeSH
- aktiny metabolismus MeSH
- aktivace enzymů MeSH
- buněčné linie MeSH
- časové faktory MeSH
- elektřina * MeSH
- fosforylace MeSH
- konexin 43 genetika metabolismus MeSH
- krysa rodu Rattus MeSH
- mezerový spoj metabolismus MeSH
- mezibuněčná komunikace * MeSH
- mitogenem aktivovaná proteinkinasa 1 metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 3 metabolismus MeSH
- mitogenem aktivované proteinkinasy p38 metabolismus MeSH
- protein zonula occludens 1 metabolismus MeSH
- regulace genové exprese MeSH
- viabilita buněk MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- aktiny MeSH
- konexin 43 MeSH
- mitogenem aktivovaná proteinkinasa 1 MeSH
- mitogenem aktivovaná proteinkinasa 3 MeSH
- mitogenem aktivované proteinkinasy p38 MeSH
- protein zonula occludens 1 MeSH
- Tjp1 protein, rat MeSH Prohlížeč
Gap junctional intercellular communication (GJIC) is an important mechanism that is involved and affected in many diseases and injuries. So far, the effect of nanosecond pulsed electric fields (nsPEFs) on the communication between cells was not investigated. An in vitro approach is presented with rat liver epithelial WB-F344 cells grown and exposed in a monolayer. In order to observe sub-lethal effects, cells were exposed to pulsed electric fields with a duration of 100ns and amplitudes between 10 and 20kV/cm. GJIC strongly decreased within 15min after treatment but recovered within 24h. Gene expression of Cx43 was significantly decreased and associated with a reduced total amount of Cx43 protein. In addition, MAP kinases p38 and Erk1/2, involved in Cx43 phosphorylation, were activated and Cx43 became hyperphosphorylated. Immunofluorescent staining of Cx43 displayed the disassembly of gap junctions. Further, a reorganization of the actin cytoskeleton was observed whereas tight junction protein ZO-1 was not significantly affected. All effects were field- and time-dependent and most pronounced within 30 to 60min after treatment. A better understanding of a possible manipulation of GJIC by nsPEFs might eventually offer a possibility to develop and improve treatments.
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