Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.

Astrocytes can tolerate longer periods of oxygen and glucose deprivation (OGD) as compared to neurons. The reasons for this reduced vulnerability are not well understood. Particularly, changes in mitochondrial membrane potential (Δψ(m)) in astrocytes, an indicator of the cellular redox state, have n...

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Autores principales:	Andrej Korenić, Johannes Boltze, Alexander Deten, Myriam Peters, Pavle Andjus, Lidija Radenović
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/056dfede10da424694fa07af77fba3b0
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spelling	oai:doaj.org-article:056dfede10da424694fa07af77fba3b02021-11-18T08:30:12ZAstrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.1932-620310.1371/journal.pone.0090697https://doaj.org/article/056dfede10da424694fa07af77fba3b02014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24587410/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Astrocytes can tolerate longer periods of oxygen and glucose deprivation (OGD) as compared to neurons. The reasons for this reduced vulnerability are not well understood. Particularly, changes in mitochondrial membrane potential (Δψ(m)) in astrocytes, an indicator of the cellular redox state, have not been investigated during reperfusion after extended OGD exposure. Here, we subjected primary mouse astrocytes to glucose deprivation (GD), OGD and combinations of both conditions varying in duration and sequence. Changes in Δψ(m), visualized by change in the fluorescence of JC-1, were investigated within one hour after reconstitution of oxygen and glucose supply, intended to model in vivo reperfusion. In all experiments, astrocytes showed resilience to extended periods of OGD, which had little effect on Δψ(m) during reperfusion, whereas GD caused a robust Δψ(m) negativation. In case no Δψ(m) negativation was observed after OGD, subsequent chemical oxygen deprivation (OD) induced by sodium azide caused depolarization, which, however, was significantly delayed as compared to normoxic group. When GD preceded OD for 12 h, Δψ(m) hyperpolarization was induced by both GD and subsequent OD, but significant interaction between these conditions was not detected. However, when GD was extended to 48 h preceding OGD, hyperpolarization enhanced during reperfusion. This implicates synergistic effects of both conditions in that sequence. These findings provide novel information regarding the role of the two main substrates of electron transport chain (glucose and oxygen) and their hyperpolarizing effect on Δψ(m) during substrate deprivation, thus shedding new light on mechanisms of astrocyte resilience to prolonged ischemic injury.Andrej KorenićJohannes BoltzeAlexander DetenMyriam PetersPavle AndjusLidija RadenovićPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 2, p e90697 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Andrej Korenić Johannes Boltze Alexander Deten Myriam Peters Pavle Andjus Lidija Radenović Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
description	Astrocytes can tolerate longer periods of oxygen and glucose deprivation (OGD) as compared to neurons. The reasons for this reduced vulnerability are not well understood. Particularly, changes in mitochondrial membrane potential (Δψ(m)) in astrocytes, an indicator of the cellular redox state, have not been investigated during reperfusion after extended OGD exposure. Here, we subjected primary mouse astrocytes to glucose deprivation (GD), OGD and combinations of both conditions varying in duration and sequence. Changes in Δψ(m), visualized by change in the fluorescence of JC-1, were investigated within one hour after reconstitution of oxygen and glucose supply, intended to model in vivo reperfusion. In all experiments, astrocytes showed resilience to extended periods of OGD, which had little effect on Δψ(m) during reperfusion, whereas GD caused a robust Δψ(m) negativation. In case no Δψ(m) negativation was observed after OGD, subsequent chemical oxygen deprivation (OD) induced by sodium azide caused depolarization, which, however, was significantly delayed as compared to normoxic group. When GD preceded OD for 12 h, Δψ(m) hyperpolarization was induced by both GD and subsequent OD, but significant interaction between these conditions was not detected. However, when GD was extended to 48 h preceding OGD, hyperpolarization enhanced during reperfusion. This implicates synergistic effects of both conditions in that sequence. These findings provide novel information regarding the role of the two main substrates of electron transport chain (glucose and oxygen) and their hyperpolarizing effect on Δψ(m) during substrate deprivation, thus shedding new light on mechanisms of astrocyte resilience to prolonged ischemic injury.
format	article
author	Andrej Korenić Johannes Boltze Alexander Deten Myriam Peters Pavle Andjus Lidija Radenović
author_facet	Andrej Korenić Johannes Boltze Alexander Deten Myriam Peters Pavle Andjus Lidija Radenović
author_sort	Andrej Korenić
title	Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
title_short	Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
title_full	Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
title_fullStr	Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
title_full_unstemmed	Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
title_sort	astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/056dfede10da424694fa07af77fba3b0
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Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.

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