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Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts
Nanoparticles are widely used in commodities, and pregnant women are inevitably exposed to these particles. The placenta protects the growing fetus from foreign or toxic materials, and provides energy and oxygen. Here we report that autophagy, a cellular mechanism to maintain homeostasis, engulfs pl...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445294/ https://www.ncbi.nlm.nih.gov/pubmed/30940860 http://dx.doi.org/10.1038/s41598-019-41927-2 |
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author | Nakashima, Akitoshi Higashisaka, Kazuma Kusabiraki, Tae Aoki, Aiko Ushijima, Akemi Ono, Yosuke Tsuda, Sayaka Shima, Tomoko Yoshino, Osamu Nagano, Kazuya Yoshioka, Yasuo Tsutsumi, Yasuo Saito, Shigeru |
author_facet | Nakashima, Akitoshi Higashisaka, Kazuma Kusabiraki, Tae Aoki, Aiko Ushijima, Akemi Ono, Yosuke Tsuda, Sayaka Shima, Tomoko Yoshino, Osamu Nagano, Kazuya Yoshioka, Yasuo Tsutsumi, Yasuo Saito, Shigeru |
author_sort | Nakashima, Akitoshi |
collection | PubMed |
description | Nanoparticles are widely used in commodities, and pregnant women are inevitably exposed to these particles. The placenta protects the growing fetus from foreign or toxic materials, and provides energy and oxygen. Here we report that autophagy, a cellular mechanism to maintain homeostasis, engulfs platinum nanoparticles (nPt) to reduce their cytotoxicity in trophoblasts. Autophagy was activated by nPt in extravillous trophoblast (EVT) cell lines, and EVT functions, such as invasion and vascular remodeling, and proliferation were inhibited by nPt. These inhibitory effects by nPt were augmented in autophagy-deficient cells. Regarding the dynamic state of nPt, analysis using ICP-MS demonstrated a higher accumulation of nPt in the autophagosome-rich than the cytoplasmic fraction in autophagy-normal cells. Meanwhile, there were more nPt in the nuclei of autophagy-deficient cells, resulting in greater DNA damage at a lower concentration of nPt. Thus, we found a new protective mechanism against the cytotoxicity of nPt in human trophoblasts. |
format | Online Article Text |
id | pubmed-6445294 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64452942019-04-08 Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts Nakashima, Akitoshi Higashisaka, Kazuma Kusabiraki, Tae Aoki, Aiko Ushijima, Akemi Ono, Yosuke Tsuda, Sayaka Shima, Tomoko Yoshino, Osamu Nagano, Kazuya Yoshioka, Yasuo Tsutsumi, Yasuo Saito, Shigeru Sci Rep Article Nanoparticles are widely used in commodities, and pregnant women are inevitably exposed to these particles. The placenta protects the growing fetus from foreign or toxic materials, and provides energy and oxygen. Here we report that autophagy, a cellular mechanism to maintain homeostasis, engulfs platinum nanoparticles (nPt) to reduce their cytotoxicity in trophoblasts. Autophagy was activated by nPt in extravillous trophoblast (EVT) cell lines, and EVT functions, such as invasion and vascular remodeling, and proliferation were inhibited by nPt. These inhibitory effects by nPt were augmented in autophagy-deficient cells. Regarding the dynamic state of nPt, analysis using ICP-MS demonstrated a higher accumulation of nPt in the autophagosome-rich than the cytoplasmic fraction in autophagy-normal cells. Meanwhile, there were more nPt in the nuclei of autophagy-deficient cells, resulting in greater DNA damage at a lower concentration of nPt. Thus, we found a new protective mechanism against the cytotoxicity of nPt in human trophoblasts. Nature Publishing Group UK 2019-04-02 /pmc/articles/PMC6445294/ /pubmed/30940860 http://dx.doi.org/10.1038/s41598-019-41927-2 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Nakashima, Akitoshi Higashisaka, Kazuma Kusabiraki, Tae Aoki, Aiko Ushijima, Akemi Ono, Yosuke Tsuda, Sayaka Shima, Tomoko Yoshino, Osamu Nagano, Kazuya Yoshioka, Yasuo Tsutsumi, Yasuo Saito, Shigeru Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title | Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title_full | Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title_fullStr | Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title_full_unstemmed | Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title_short | Autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
title_sort | autophagy is a new protective mechanism against the cytotoxicity of platinum nanoparticles in human trophoblasts |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445294/ https://www.ncbi.nlm.nih.gov/pubmed/30940860 http://dx.doi.org/10.1038/s41598-019-41927-2 |
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