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

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...

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Autores principales: Chen, Chen-Mei, Wu, Meng-Ling, Ho, Yen-Chun, Gung, Pei-Yu, Tsai, Ming-Hsien, Orekhov, Alexander N., Sobenin, Igor A., Lin, Pinpin, Yet, Shaw-Fang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279309/
https://www.ncbi.nlm.nih.gov/pubmed/32414036
http://dx.doi.org/10.3390/ijms21103437
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author Chen, Chen-Mei
Wu, Meng-Ling
Ho, Yen-Chun
Gung, Pei-Yu
Tsai, Ming-Hsien
Orekhov, Alexander N.
Sobenin, Igor A.
Lin, Pinpin
Yet, Shaw-Fang
author_facet Chen, Chen-Mei
Wu, Meng-Ling
Ho, Yen-Chun
Gung, Pei-Yu
Tsai, Ming-Hsien
Orekhov, Alexander N.
Sobenin, Igor A.
Lin, Pinpin
Yet, Shaw-Fang
author_sort Chen, Chen-Mei
collection PubMed
description 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.
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spelling pubmed-72793092020-06-17 Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration Chen, Chen-Mei Wu, Meng-Ling Ho, Yen-Chun Gung, Pei-Yu Tsai, Ming-Hsien Orekhov, Alexander N. Sobenin, Igor A. Lin, Pinpin Yet, Shaw-Fang Int J Mol Sci Article 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. MDPI 2020-05-13 /pmc/articles/PMC7279309/ /pubmed/32414036 http://dx.doi.org/10.3390/ijms21103437 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Chen, Chen-Mei
Wu, Meng-Ling
Ho, Yen-Chun
Gung, Pei-Yu
Tsai, Ming-Hsien
Orekhov, Alexander N.
Sobenin, Igor A.
Lin, Pinpin
Yet, Shaw-Fang
Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title_full Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title_fullStr Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title_full_unstemmed Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title_short Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration
title_sort exposure to zinc oxide nanoparticles disrupts endothelial tight and adherens junctions and induces pulmonary inflammatory cell infiltration
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279309/
https://www.ncbi.nlm.nih.gov/pubmed/32414036
http://dx.doi.org/10.3390/ijms21103437
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