ArticleParticle and fibre toxicology2018
Developmental basis for intestinal barrier against the toxicity of graphene oxide.
Article in Particle and fibre toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 77 citations in OpenAlex.
- Baicalein fromFrontiers in pharmacology · 2025Article
- Engineering the surface of graphene oxide with bovine serum albumin for improved biocompatibility inNanoscale advances · 2020Article
- Inhibition of in-stent restenosis after graphene oxide double-layer drug coating with good biocompatibility.Regenerative biomaterials · 2019Article
- A circular RNARSC advances · 2019Article
- Biosafety assessment of water samples from Wanzhou watershed of Yangtze Three Gorges Reservior in the quiet season in Caenorhabditis elegans.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIntestinal barrier is crucial for animals against translocation of engineered nanomaterials (ENMs) into secondary targeted organs. However, the molecular mechanisms for the role of intestinal barrier against ENMs toxicity are still largely unclear. The intestine of Caenorhabditis elegans is a powerful in vivo experimental system for the study on intestinal function. In this study, we investigated the molecular basis for intestinal barrier against toxicity and translocation of graphene oxide (GO) using C. elegans as a model animal.
resultsBased on the genetic screen of genes required for the control of intestinal development at different aspects using intestine-specific RNA interference (RNAi) technique, we identified four genes (erm-1, pkc-3, hmp-2 and act-5) required for the function of intestinal barrier against GO toxicity. Under normal conditions, mutation of any of these genes altered the intestinal permeability. With the focus on PKC-3, an atypical protein kinase C, we identified an intestinal signaling cascade of PKC-3-SEC-8-WTS-1, which implies that PKC-3 might regulate intestinal permeability and GO toxicity by affecting the function of SEC-8-mediated exocyst complex and the role of WTS-1 in maintaining integrity of apical intestinal membrane. ISP-1 and SOD-3, two proteins required for the control of oxidative stress, were also identified as downstream targets for PKC-3, and functioned in parallel with WTS-1 in the regulation of GO toxicity.
conclusionsUsing C. elegans as an in vivo assay system, we found that several developmental genes required for the control of intestinal development regulated both the intestinal permeability and the GO toxicity. With the focus on PKC-3, we raised two intestinal signaling cascades, PKC-3-SEC-8-WTS-1 and PKC-3-ISP-1/SOD-3. Our results will strengthen our understanding the molecular basis for developmental machinery of intestinal barrier against GO toxicity and translocation in animals.
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Registered trials
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