Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration.

Autor: Chen CM; Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 35053, Taiwan., Wu ML; Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 35053, Taiwan., Ho YC; Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 35053, Taiwan., Gung PY; Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 35053, Taiwan., Tsai MH; National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan 35053, Taiwan., Orekhov AN; Institute of Human Morphology, 3 Tsyurupa Street, Moscow 117418, Russia., Sobenin IA; Laboratory of Medical Genetics, National Medical Research Center of Cardiology, 15A 3-rd Cherepkovskaya Street, Moscow 121552, Russia., Lin P; National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan 35053, Taiwan., Yet SF; Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 35053, Taiwan.; Graduate Institute of Biomedical Sciences, China Medical University, Taichung 40402, Taiwan.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2020 May 13; Vol. 21 (10). Date of Electronic Publication: 2020 May 13.
DOI: 10.3390/ijms21103437
Abstrakt: Zinc oxide nanoparticles (ZnONPs) are frequently encountered nanomaterials in our daily lives. Despite the benefits of ZnONPs in a variety of applications, many studies have shown potential health hazards of exposure to ZnONPs. We have shown that oropharyngeal aspiration of ZnONPs in mice increases lung inflammation. However, the detailed mechanisms underlying pulmonary inflammatory cell infiltration remain to be elucidated. Endothelium functions as a barrier between the blood stream and the blood vessel wall. Endothelial barrier dysfunction may increase infiltration of immune cells into the vessel wall and underlying tissues. This current study examined the effects of ZnONPs exposure on endothelial barriers. ZnONPs exposure increased leukocyte infiltration in the mouse lungs. In endothelial cells, ZnONPs reduced the continuity of tight junction proteins claudin-5 and zonula occludens-1 (ZO-1) at the cell junctions. ZnONPs induced adherens junction protein VE-cadherin internalization from membrane to cytosol and dissociation with β-catenin, leading to reduced and diffused staining of VE-cadherin and β-catenin at cell junctions. Our results demonstrated that ZnONPs disrupted both tight and adherens junctions, compromising the integrity and stability of the junction network, leading to inflammatory cell infiltration. Thus, ZnONPs exposure in many different settings should be carefully evaluated for vascular effects and subsequent health impacts.
Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results”.
Databáze: MEDLINE
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