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Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke
Ring finger protein 146 (Iduna) facilitates DNA repair and protects against cell death induced by NMDA receptor-mediated glutamate excitotoxicity or by cerebral ischemia. Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived lipid mediator, promotes cell survival under uncompensated oxidati...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442474/ https://www.ncbi.nlm.nih.gov/pubmed/28430183 http://dx.doi.org/10.1038/cdd.2017.55 |
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author | Belayev, Ludmila Mukherjee, Pranab K Balaszczuk, Veronica Calandria, Jorgelina M Obenaus, Andre Khoutorova, Larissa Hong, Sung-Ha Bazan, Nicolas G |
author_facet | Belayev, Ludmila Mukherjee, Pranab K Balaszczuk, Veronica Calandria, Jorgelina M Obenaus, Andre Khoutorova, Larissa Hong, Sung-Ha Bazan, Nicolas G |
author_sort | Belayev, Ludmila |
collection | PubMed |
description | Ring finger protein 146 (Iduna) facilitates DNA repair and protects against cell death induced by NMDA receptor-mediated glutamate excitotoxicity or by cerebral ischemia. Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived lipid mediator, promotes cell survival under uncompensated oxidative stress (UOS). Our data demonstrate that NPD1 potently upregulates Iduna expression and provides remarkable cell protection against UOS. Iduna, which was increased by the lipid mediator, requires the presence of the poly(ADP-ribose) (PAR) sites. Moreover, astrocytes and neurons in the penumbra display an enhanced abundance of Iduna, followed by remarkable neurological protection when DHA, a precursor of NPD1, is systemically administered 1 h after 2 h of ischemic stroke. These findings provide a conceptual advancement for survival of neural cells undergoing challenges to homeostasis because a lipid mediator, made 'on demand,' modulates the abundance of a critically important protein for cell survival. |
format | Online Article Text |
id | pubmed-5442474 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-54424742017-06-03 Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke Belayev, Ludmila Mukherjee, Pranab K Balaszczuk, Veronica Calandria, Jorgelina M Obenaus, Andre Khoutorova, Larissa Hong, Sung-Ha Bazan, Nicolas G Cell Death Differ Original Paper Ring finger protein 146 (Iduna) facilitates DNA repair and protects against cell death induced by NMDA receptor-mediated glutamate excitotoxicity or by cerebral ischemia. Neuroprotectin D1 (NPD1), a docosahexaenoic acid (DHA)-derived lipid mediator, promotes cell survival under uncompensated oxidative stress (UOS). Our data demonstrate that NPD1 potently upregulates Iduna expression and provides remarkable cell protection against UOS. Iduna, which was increased by the lipid mediator, requires the presence of the poly(ADP-ribose) (PAR) sites. Moreover, astrocytes and neurons in the penumbra display an enhanced abundance of Iduna, followed by remarkable neurological protection when DHA, a precursor of NPD1, is systemically administered 1 h after 2 h of ischemic stroke. These findings provide a conceptual advancement for survival of neural cells undergoing challenges to homeostasis because a lipid mediator, made 'on demand,' modulates the abundance of a critically important protein for cell survival. Nature Publishing Group 2017-06 2017-04-21 /pmc/articles/PMC5442474/ /pubmed/28430183 http://dx.doi.org/10.1038/cdd.2017.55 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Original Paper Belayev, Ludmila Mukherjee, Pranab K Balaszczuk, Veronica Calandria, Jorgelina M Obenaus, Andre Khoutorova, Larissa Hong, Sung-Ha Bazan, Nicolas G Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title | Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title_full | Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title_fullStr | Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title_full_unstemmed | Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title_short | Neuroprotectin D1 upregulates Iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
title_sort | neuroprotectin d1 upregulates iduna expression and provides protection in cellular uncompensated oxidative stress and in experimental ischemic stroke |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442474/ https://www.ncbi.nlm.nih.gov/pubmed/28430183 http://dx.doi.org/10.1038/cdd.2017.55 |
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