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SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport
Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance “big” K(+) channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposure to volatile anesthetics initiates protection ag...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228735/ https://www.ncbi.nlm.nih.gov/pubmed/22145034 http://dx.doi.org/10.1371/journal.pone.0028287 |
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author | Wojtovich, Andrew P. Sherman, Teresa A. Nadtochiy, Sergiy M. Urciuoli, William R. Brookes, Paul S. Nehrke, Keith |
author_facet | Wojtovich, Andrew P. Sherman, Teresa A. Nadtochiy, Sergiy M. Urciuoli, William R. Brookes, Paul S. Nehrke, Keith |
author_sort | Wojtovich, Andrew P. |
collection | PubMed |
description | Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance “big” K(+) channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposure to volatile anesthetics initiates protection against ischemic injury. Despite the role of the mBK in cardioprotection, the molecular identity of the channel remains unknown. We investigated the attributes of the mBK using C. elegans and mouse genetic models coupled with measurements of mitochondrial K(+) transport and APC. The canonical Ca(2+)-activated BK (or “maxi-K”) channel SLO1 was dispensable for both mitochondrial K(+) transport and APC in both organisms. Instead, we found that the related but physiologically-distinct K(+) channel SLO2 was required, and that SLO2-dependent mitochondrial K(+) transport was triggered directly by volatile anesthetics. In addition, a SLO2 channel activator mimicked the protective effects of volatile anesthetics. These findings suggest that SLO2 contributes to protection from hypoxic injury by increasing the permeability of the mitochondrial inner membrane to K(+). |
format | Online Article Text |
id | pubmed-3228735 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-32287352011-12-05 SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport Wojtovich, Andrew P. Sherman, Teresa A. Nadtochiy, Sergiy M. Urciuoli, William R. Brookes, Paul S. Nehrke, Keith PLoS One Research Article Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance “big” K(+) channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposure to volatile anesthetics initiates protection against ischemic injury. Despite the role of the mBK in cardioprotection, the molecular identity of the channel remains unknown. We investigated the attributes of the mBK using C. elegans and mouse genetic models coupled with measurements of mitochondrial K(+) transport and APC. The canonical Ca(2+)-activated BK (or “maxi-K”) channel SLO1 was dispensable for both mitochondrial K(+) transport and APC in both organisms. Instead, we found that the related but physiologically-distinct K(+) channel SLO2 was required, and that SLO2-dependent mitochondrial K(+) transport was triggered directly by volatile anesthetics. In addition, a SLO2 channel activator mimicked the protective effects of volatile anesthetics. These findings suggest that SLO2 contributes to protection from hypoxic injury by increasing the permeability of the mitochondrial inner membrane to K(+). Public Library of Science 2011-12-01 /pmc/articles/PMC3228735/ /pubmed/22145034 http://dx.doi.org/10.1371/journal.pone.0028287 Text en Wojtovich et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Wojtovich, Andrew P. Sherman, Teresa A. Nadtochiy, Sergiy M. Urciuoli, William R. Brookes, Paul S. Nehrke, Keith SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title | SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title_full | SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title_fullStr | SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title_full_unstemmed | SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title_short | SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport |
title_sort | slo-2 is cytoprotective and contributes to mitochondrial potassium transport |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228735/ https://www.ncbi.nlm.nih.gov/pubmed/22145034 http://dx.doi.org/10.1371/journal.pone.0028287 |
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