Graphene oxide (GO), one kind of promising engineered nanomaterials (ENM), is extensively applied to biomedical fields such as optical imaging and drug delivery, and could be used as a chemical sensor. Many studies have focused on toxicity effects of GO, however, the underlying mechanisms remain unclear, especially from the perspective of epigenetic regulation.
Recently, WU Lijun's group at Hefei Institutes of Physical Science of Chinese Academy of Sciences revealed mechanisms underlying graphene oxide-triggered toxicity in human embryonic kidney 293T Cells using chromosome conformation capture technology. The finding was published in Nanotoxicology.
The researchers investigated the role of GO-triggered chromatin interactions in the activation of cox2, a hallmark of inflammation, in normal human cells. The results showed that GO triggers physical interactions between the downstream enhancer and the cox2 promoter in human embryonic kidney 293T (293T) via p65 and p300 complex-mediated dynamic chromatin looping, which was required for high cox2 expression.
Moreover, tumor necrosis factor-α (TNF-α) was found to contribute to the regulation of cox2 activation through dynamic chromatin architecture. Compared with pristine GO and GO-NH2, GO-PAA induced a weaker inflammatory response and a weaker effect on chromatin architecture.
This study mechanistically linked GO-mediated chromatin interactions to the regulation of cox2 and suggested that GO derivatives may minimize toxicity in practical applications.
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