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Difference between revisions of "Bergmeister 2022 Abstract Bioblast"

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(Created page with "{{Abstract |title=Bergmeister L, Doerrier C, Gnaiger E, Schwarzer C (2022) The role of enkephalin in hypoxic preconditioning. Bioblast 2022: BEC Inaugural Conference. |info=[h...")
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|info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference]
|info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference]
|authors=Bergmeister Lisa, Doerrier Carolina, Gnaiger Erich, Schwarzer Christoph
|authors=Bergmeister Lisa, Doerrier Carolina, Gnaiger Erich, Schwarzer Christoph
|year=2022
|event=[[Bioblast 2022]]
|abstract=Hypoxic preconditioning (HPC) is the application of mild transient hypoxia which protects the brain against a following more severe hypoxic insult as it occurs during epileptic seizures. HPC decreases seizure susceptibility and severity as well as neuronal damage in the hippocampus. The delta opioid receptor (DOR) and its primary endogenous ligands, the neuropeptides met- and leu-enkephalin (Enk), are thought to be involved in the neuroprotective actions of HPC. Recently, we showed that Enk influences mitochondrial respiration that may contribute to the neuroprotective effects of the Enk/DOR system. The present study aims at investigating the effects of the Enk/DOR system on structural and functional alterations of mitochondria in HPC.


|year=2022
Wild type (WT) and met-Enk-knockout (met-Enk-KO) mice were exposed to hypoxia. Subsequently, we determined the seizure threshold, analyzed mitochondrial function and dynamics.


|event=[[Bioblast 2022]]
In WT mice after HPC we observed an elevated seizure threshold, improved mitochondrial reserve capacity and increased mitochondrial fusion. In addition, our results suggest mitochondrial biogenesis after HPC in WT mice. NaΓ―ve met-Enk-KO mice had an increased seizure threshold and increased mitochondrial fusion but no changes upon HPC.
|abstract=
Background: Hypoxic preconditioning (HPC) is the application of mild transient hypoxia which protects the brain against a following more severe hypoxic insult as it occurs during epileptic seizures. HPC decreases seizure susceptibility and severity as well as neuronal damage in the hippocampus. The delta opioid receptor (DOR) and its primary endogenous ligands, the neuropeptides met- and leu-enkephalin (Enk), are thought to be involved in the neuroprotective actions of HPC. Recently, we showed that Enk influences mitochondrial respiration that may contribute to the neuroprotective effects of the Enk/DOR system. The present study aims at investigating the effects of the Enk/DOR system on structural and functional alterations of mitochondria in HPC.
<br>
Methods: Wild type (WT) and met-Enk-knockout (met-Enk-KO) mice were exposed to hypoxia. Subsequently, we determined the seizure threshold, analyzed mitochondrial function and dynamics.
<br>
Results: In WT mice after HPC we observed an elevated seizure threshold, improved mitochondrial reserve capacity and increased mitochondrial fusion. In addition, our results suggest mitochondrial biogenesis after HPC in WT mice. NaΓ―ve met-Enk-KO mice had an increased seizure threshold and increased mitochondrial fusion but no changes upon HPC.
<br>
Conclusion: The observed mitochondrial alterations after HPC in WT mice could explain improved neuronal survival and increased seizure threshold. Enhanced mitochondrial reserve capacity improves energy supply in stress situations and increased mitochondrial fusion is associated with neuronal survival and elevated Ca2+ storage capacities. However, the precise role of met-Enk in HPC is unclear but we observed adaptive mechanisms in WT mice upon hypoxia which are absent in met-Enk-KO mice.


The observed mitochondrial alterations after HPC in WT mice could explain improved neuronal survival and increased seizure threshold. Enhanced mitochondrial reserve capacity improves energy supply in stress situations and increased mitochondrial fusion is associated with neuronal survival and elevated Ca2+ storage capacities. However, the precise role of met-Enk in HPC is unclear but we observed adaptive mechanisms in WT mice upon hypoxia which are absent in met-Enk-KO mice.
|keywords=Mitochondrial disorders, Leigh syndrome, Glycolysis, Mitochondrial respiration, Bioenergetics health index
|keywords=Mitochondrial disorders, Leigh syndrome, Glycolysis, Mitochondrial respiration, Bioenergetics health index
|editor=
|mipnetlab=AT Innsbruck Oroboros
|mipnetlab=AT Innsbruck Oroboros
|articletype=Abstract
|articletype=Abstract
}}
}}
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{{Labeling
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== Affiliations ==
== Affiliations and support ==
::::Bergmeister L(1), Doerrier C(2), Gnaiger(2) and Schwarzer C(1)
::::Bergmeister L(1), Doerrier C(2), Gnaiger(2) and Schwarzer C(1)
::::#Department of Pharmacology, Medical University of Innsbruck, Innsbruck, Austria
::::#Department of Pharmacology, Medical University of Innsbruck, Innsbruck, Austria
::::#Oroboros Instruments GmbH, Innsbruck, Austria
::::#Oroboros Instruments GmbH, Innsbruck, Austria
== Acknowledgements ==


::::This study is supported by the Austrian Science Fund FWF (SPIN W-1206) and Oroboros Instruments GmbH.
::::This study is supported by the Austrian Science Fund FWF (SPIN W-1206) and Oroboros Instruments GmbH.

Revision as of 14:45, 12 May 2022

Bergmeister L, Doerrier C, Gnaiger E, Schwarzer C (2022) The role of enkephalin in hypoxic preconditioning. Bioblast 2022: BEC Inaugural Conference.

Link: Bioblast 2022: BEC Inaugural Conference

Bergmeister Lisa, Doerrier Carolina, Gnaiger Erich, Schwarzer Christoph (2022)

Event: Bioblast 2022

Hypoxic preconditioning (HPC) is the application of mild transient hypoxia which protects the brain against a following more severe hypoxic insult as it occurs during epileptic seizures. HPC decreases seizure susceptibility and severity as well as neuronal damage in the hippocampus. The delta opioid receptor (DOR) and its primary endogenous ligands, the neuropeptides met- and leu-enkephalin (Enk), are thought to be involved in the neuroprotective actions of HPC. Recently, we showed that Enk influences mitochondrial respiration that may contribute to the neuroprotective effects of the Enk/DOR system. The present study aims at investigating the effects of the Enk/DOR system on structural and functional alterations of mitochondria in HPC.

Wild type (WT) and met-Enk-knockout (met-Enk-KO) mice were exposed to hypoxia. Subsequently, we determined the seizure threshold, analyzed mitochondrial function and dynamics.

In WT mice after HPC we observed an elevated seizure threshold, improved mitochondrial reserve capacity and increased mitochondrial fusion. In addition, our results suggest mitochondrial biogenesis after HPC in WT mice. NaΓ―ve met-Enk-KO mice had an increased seizure threshold and increased mitochondrial fusion but no changes upon HPC.

The observed mitochondrial alterations after HPC in WT mice could explain improved neuronal survival and increased seizure threshold. Enhanced mitochondrial reserve capacity improves energy supply in stress situations and increased mitochondrial fusion is associated with neuronal survival and elevated Ca2+ storage capacities. However, the precise role of met-Enk in HPC is unclear but we observed adaptive mechanisms in WT mice upon hypoxia which are absent in met-Enk-KO mice.

β€’ Keywords: Mitochondrial disorders, Leigh syndrome, Glycolysis, Mitochondrial respiration, Bioenergetics health index

β€’ O2k-Network Lab: AT Innsbruck Oroboros


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Affiliations and support

Bergmeister L(1), Doerrier C(2), Gnaiger(2) and Schwarzer C(1)
  1. Department of Pharmacology, Medical University of Innsbruck, Innsbruck, Austria
  2. Oroboros Instruments GmbH, Innsbruck, Austria
This study is supported by the Austrian Science Fund FWF (SPIN W-1206) and Oroboros Instruments GmbH.

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