期刊
JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
卷 15, 期 3, 页码 443-461出版社
AMER SCIENTIFIC PUBLISHERS
DOI: 10.1166/jbn.2019.2696
关键词
Zinc Oxide Nanoparticles; Endothelial Barrier; Interendothelial Junctions; Endocytosis
资金
- National Key Research and Development Program of China [2016YFC1102605, 2016YFC1102603]
- Shenzhen Technology Innovation Project [JSGG20170412145203293]
- Shenzhen Basic Research Project [JCYJ20170815153143221]
In this study, the effects of zinc oxide nanoparticle (ZnO-NP) exposure on the endothelial barrier and the pathway of ZnO-NPs to cross the endothelial barrier were examined. C57 mice were exposed to ZnO-NPs (1.2 mg/kg and 6 mg/kg body weight) and ZnSO4 (3.6 mg/kg). Zinc biodistribution and toxicity tests, including H&E staining, TUNEL and 8-OHdG IHC staining of highly vascularized organs (liver, kidney and spleen), were assessed. Endothelial barrier disruption was assessed by interendothelial junction IHC staining of the thoracic aorta, and was further studied in human umbilical vein endothelial cells (HUVECs). Four different kinds of endocytosis inhibitors were also used to study the endocytosis effects of the ZnO-NPs on the HUVECs. We found that a significantly increased concentration of zinc was detected in the highly vascularized organs from the ZnO-NP exposure groups, together with histopathologic changes such as higher apoptotic death and oxidative status. Interendothelial junction disruption and increased endothelial barrier permeability were found in both the in vivo and in vitro experiments. All four endocytosis inhibitors were able to reduce the uptake and transport of ZnO-NPs in the HUVECs. We concluded that ZnO-NPs may impair endothelial cells and induce endothelial barrier dysfunction and are able to cross the endothelial barrier through paracellular and transcellular routes.
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