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Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways
BACKGROUND: Deinococcus radiodurans is a robust bacterium that can withstand harsh environments that cause oxidative stress to macromolecules due to its cellular structure and physiological functions. Cells release extracellular vesicles for intercellular communication and the transfer of biological...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10273539/ https://www.ncbi.nlm.nih.gov/pubmed/37328878 http://dx.doi.org/10.1186/s12575-023-00211-4 |
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author | Han, Jeong Moo Song, Ha-Yeon Jung, Jong-Hyun Lim, Sangyong Seo, Ho Seong Kim, Woo Sik Lim, Seung-Taik Byun, Eui-Baek |
author_facet | Han, Jeong Moo Song, Ha-Yeon Jung, Jong-Hyun Lim, Sangyong Seo, Ho Seong Kim, Woo Sik Lim, Seung-Taik Byun, Eui-Baek |
author_sort | Han, Jeong Moo |
collection | PubMed |
description | BACKGROUND: Deinococcus radiodurans is a robust bacterium that can withstand harsh environments that cause oxidative stress to macromolecules due to its cellular structure and physiological functions. Cells release extracellular vesicles for intercellular communication and the transfer of biological information; their payload reflects the status of the source cells. Yet, the biological role and mechanism of Deinococcus radiodurans-derived extracellular vesicles remain unclear. AIM: This study investigated the protective effects of membrane vesicles derived from D. radiodurans (R1-MVs) against H(2)O(2)-induced oxidative stress in HaCaT cells. RESULTS: R1-MVs were identified as 322 nm spherical molecules. Pretreatment with R1-MVs inhibited H(2)O(2)-mediated apoptosis in HaCaT cells by suppressing the loss of mitochondrial membrane potential and reactive oxygen species (ROS) production. R1-MVs increased the superoxide dismutase (SOD) and catalase (CAT) activities, restored glutathione (GSH) homeostasis, and reduced malondialdehyde (MDA) production in H(2)O(2)-exposed HaCaT cells. Moreover, the protective effect of R1-MVs against H(2)O(2)-induced oxidative stress in HaCaT cells was dependent on the downregulation of mitogen-activated protein kinase (MAPK) phosphorylation and the upregulation of the nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway. Furthermore, the weaker protective capabilities of R1-MVs derived from ΔDR2577 mutant than that of the wild-type R1-MVs confirmed our inferences and indicated that SlpA protein plays a crucial role in R1-MVs against H(2)O(2)-induced oxidative stress. CONCLUSION: Taken together, R1-MVs exert significant protective effects against H(2)O(2)-induced oxidative stress in keratinocytes and have the potential to be applied in radiation-induced oxidative stress models. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12575-023-00211-4. |
format | Online Article Text |
id | pubmed-10273539 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-102735392023-06-17 Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways Han, Jeong Moo Song, Ha-Yeon Jung, Jong-Hyun Lim, Sangyong Seo, Ho Seong Kim, Woo Sik Lim, Seung-Taik Byun, Eui-Baek Biol Proced Online Research BACKGROUND: Deinococcus radiodurans is a robust bacterium that can withstand harsh environments that cause oxidative stress to macromolecules due to its cellular structure and physiological functions. Cells release extracellular vesicles for intercellular communication and the transfer of biological information; their payload reflects the status of the source cells. Yet, the biological role and mechanism of Deinococcus radiodurans-derived extracellular vesicles remain unclear. AIM: This study investigated the protective effects of membrane vesicles derived from D. radiodurans (R1-MVs) against H(2)O(2)-induced oxidative stress in HaCaT cells. RESULTS: R1-MVs were identified as 322 nm spherical molecules. Pretreatment with R1-MVs inhibited H(2)O(2)-mediated apoptosis in HaCaT cells by suppressing the loss of mitochondrial membrane potential and reactive oxygen species (ROS) production. R1-MVs increased the superoxide dismutase (SOD) and catalase (CAT) activities, restored glutathione (GSH) homeostasis, and reduced malondialdehyde (MDA) production in H(2)O(2)-exposed HaCaT cells. Moreover, the protective effect of R1-MVs against H(2)O(2)-induced oxidative stress in HaCaT cells was dependent on the downregulation of mitogen-activated protein kinase (MAPK) phosphorylation and the upregulation of the nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway. Furthermore, the weaker protective capabilities of R1-MVs derived from ΔDR2577 mutant than that of the wild-type R1-MVs confirmed our inferences and indicated that SlpA protein plays a crucial role in R1-MVs against H(2)O(2)-induced oxidative stress. CONCLUSION: Taken together, R1-MVs exert significant protective effects against H(2)O(2)-induced oxidative stress in keratinocytes and have the potential to be applied in radiation-induced oxidative stress models. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12575-023-00211-4. BioMed Central 2023-06-16 /pmc/articles/PMC10273539/ /pubmed/37328878 http://dx.doi.org/10.1186/s12575-023-00211-4 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Han, Jeong Moo Song, Ha-Yeon Jung, Jong-Hyun Lim, Sangyong Seo, Ho Seong Kim, Woo Sik Lim, Seung-Taik Byun, Eui-Baek Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title | Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title_full | Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title_fullStr | Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title_full_unstemmed | Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title_short | Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H(2)O(2)-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways |
title_sort | deinococcus radiodurans-derived membrane vesicles protect hacat cells against h(2)o(2)-induced oxidative stress via modulation of mapk and nrf2/are pathways |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10273539/ https://www.ncbi.nlm.nih.gov/pubmed/37328878 http://dx.doi.org/10.1186/s12575-023-00211-4 |
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