SUMO2/3 conjugation is an endogenous neuroprotective mechanism

Small ubiquitin-like modifier (SUMO)2/3 but not SUMO1 conjugation is activated after transient cerebral ischemia. To investigate its function, we blocked neuronal SUMO2/3 translation through lentiviral microRNA delivery in primary cortical neurons. Viability was unaffected by SUMO2/3 silencing unles...

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Autores principales: Datwyler, Anna Lena, Lättig-Tünnemann, Gisela, Yang, Wei, Paschen, Wulf, Lee, Sabrina Lin Lin, Dirnagl, Ulrich, Endres, Matthias, Harms, Christoph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Brief Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210338/
https://www.ncbi.nlm.nih.gov/pubmed/21863037
http://dx.doi.org/10.1038/jcbfm.2011.112
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author Datwyler, Anna Lena
Lättig-Tünnemann, Gisela
Yang, Wei
Paschen, Wulf
Lee, Sabrina Lin Lin
Dirnagl, Ulrich
Endres, Matthias
Harms, Christoph
author_facet Datwyler, Anna Lena
Lättig-Tünnemann, Gisela
Yang, Wei
Paschen, Wulf
Lee, Sabrina Lin Lin
Dirnagl, Ulrich
Endres, Matthias
Harms, Christoph
author_sort Datwyler, Anna Lena
collection PubMed
description Small ubiquitin-like modifier (SUMO)2/3 but not SUMO1 conjugation is activated after transient cerebral ischemia. To investigate its function, we blocked neuronal SUMO2/3 translation through lentiviral microRNA delivery in primary cortical neurons. Viability was unaffected by SUMO2/3 silencing unless neurons were stressed by transient oxygen–glucose deprivation (OGD). Both 15 and 45 minutes of OGD were tolerated by control microRNA-expressing neurons but damaged >60% of neurons expressing SUMO2/3 microRNA. Damaging OGD (75 minutes) increased neuronal loss to 54% (control microRNA) and to 99% (SUMO2/3 microRNA). This suggests that activation of SUMO2/3 conjugation is an endogenous neuroprotective stress response.
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spelling pubmed-32103382011-11-30 SUMO2/3 conjugation is an endogenous neuroprotective mechanism Datwyler, Anna Lena Lättig-Tünnemann, Gisela Yang, Wei Paschen, Wulf Lee, Sabrina Lin Lin Dirnagl, Ulrich Endres, Matthias Harms, Christoph J Cereb Blood Flow Metab Brief Communication Small ubiquitin-like modifier (SUMO)2/3 but not SUMO1 conjugation is activated after transient cerebral ischemia. To investigate its function, we blocked neuronal SUMO2/3 translation through lentiviral microRNA delivery in primary cortical neurons. Viability was unaffected by SUMO2/3 silencing unless neurons were stressed by transient oxygen–glucose deprivation (OGD). Both 15 and 45 minutes of OGD were tolerated by control microRNA-expressing neurons but damaged >60% of neurons expressing SUMO2/3 microRNA. Damaging OGD (75 minutes) increased neuronal loss to 54% (control microRNA) and to 99% (SUMO2/3 microRNA). This suggests that activation of SUMO2/3 conjugation is an endogenous neuroprotective stress response. Nature Publishing Group 2011-11 2011-08-24 /pmc/articles/PMC3210338/ /pubmed/21863037 http://dx.doi.org/10.1038/jcbfm.2011.112 Text en Copyright © 2011 International Society for Cerebral Blood Flow & Metabolism, Inc. http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Brief Communication
Datwyler, Anna Lena
Lättig-Tünnemann, Gisela
Yang, Wei
Paschen, Wulf
Lee, Sabrina Lin Lin
Dirnagl, Ulrich
Endres, Matthias
Harms, Christoph
SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title_full SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title_fullStr SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title_full_unstemmed SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title_short SUMO2/3 conjugation is an endogenous neuroprotective mechanism
title_sort sumo2/3 conjugation is an endogenous neuroprotective mechanism
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210338/
https://www.ncbi.nlm.nih.gov/pubmed/21863037
http://dx.doi.org/10.1038/jcbfm.2011.112
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