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Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism of SUR2A-mediated cytoprotection independent from the K(ATP) channel activity
Transgenic mice overexpressing SUR2A, a subunit of ATP-sensitive K(+) (K(ATP)) channels, acquire resistance to myocardial ischaemia. However, the mechanism of SUR2A-mediated cytoprotection is yet to be fully understood. Adenoviral SUR2A construct (AV-SUR2A) increased SUR2A expression, number of K(AT...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Elsevier Pub. Co
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881534/ https://www.ncbi.nlm.nih.gov/pubmed/20123112 http://dx.doi.org/10.1016/j.bbamcr.2010.01.018 |
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author | Du, Qingyou Jovanović, Sofija Sukhodub, Andriy Jovanović, Aleksandar |
author_facet | Du, Qingyou Jovanović, Sofija Sukhodub, Andriy Jovanović, Aleksandar |
author_sort | Du, Qingyou |
collection | PubMed |
description | Transgenic mice overexpressing SUR2A, a subunit of ATP-sensitive K(+) (K(ATP)) channels, acquire resistance to myocardial ischaemia. However, the mechanism of SUR2A-mediated cytoprotection is yet to be fully understood. Adenoviral SUR2A construct (AV-SUR2A) increased SUR2A expression, number of K(ATP) channels and subsarcolemmal ATP in glycolysis-sensitive manner in H9C2 cells. It also increased K(+) current in response to chemical hypoxia, partially preserved subsarcolemmal ATP and increased cell survival. Kir6.2AFA, a mutant form of Kir6.2 with largely decreased K(+) conductance, abolished the effect of SUR2A on K(+) current, did not affect SUR2A-induced increase in subsarcolemmal ATP and partially inhibited SUR2A-mediated cytoprotection. Infection with 193gly-M-LDH, an inactive mutant of muscle lactate dehydrogenase, abolished the effect of SUR2A on K(+) current, subsarcolemmal ATP and cell survival; the effect of 193gly-M-LDH on cell survival was significantly more pronounced than those of Kir6.2AFA. We conclude that AV-SUR2A increases resistance to metabolic stress in H9C2 cells by increasing the number of sarcolemmal K(ATP) channels and subsarcolemmal ATP. |
format | Text |
id | pubmed-2881534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Elsevier Pub. Co |
record_format | MEDLINE/PubMed |
spelling | pubmed-28815342010-06-07 Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism of SUR2A-mediated cytoprotection independent from the K(ATP) channel activity Du, Qingyou Jovanović, Sofija Sukhodub, Andriy Jovanović, Aleksandar Biochim Biophys Acta Article Transgenic mice overexpressing SUR2A, a subunit of ATP-sensitive K(+) (K(ATP)) channels, acquire resistance to myocardial ischaemia. However, the mechanism of SUR2A-mediated cytoprotection is yet to be fully understood. Adenoviral SUR2A construct (AV-SUR2A) increased SUR2A expression, number of K(ATP) channels and subsarcolemmal ATP in glycolysis-sensitive manner in H9C2 cells. It also increased K(+) current in response to chemical hypoxia, partially preserved subsarcolemmal ATP and increased cell survival. Kir6.2AFA, a mutant form of Kir6.2 with largely decreased K(+) conductance, abolished the effect of SUR2A on K(+) current, did not affect SUR2A-induced increase in subsarcolemmal ATP and partially inhibited SUR2A-mediated cytoprotection. Infection with 193gly-M-LDH, an inactive mutant of muscle lactate dehydrogenase, abolished the effect of SUR2A on K(+) current, subsarcolemmal ATP and cell survival; the effect of 193gly-M-LDH on cell survival was significantly more pronounced than those of Kir6.2AFA. We conclude that AV-SUR2A increases resistance to metabolic stress in H9C2 cells by increasing the number of sarcolemmal K(ATP) channels and subsarcolemmal ATP. Elsevier Pub. Co 2010-03 /pmc/articles/PMC2881534/ /pubmed/20123112 http://dx.doi.org/10.1016/j.bbamcr.2010.01.018 Text en © 2010 Elsevier B.V. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license |
spellingShingle | Article Du, Qingyou Jovanović, Sofija Sukhodub, Andriy Jovanović, Aleksandar Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism of SUR2A-mediated cytoprotection independent from the K(ATP) channel activity |
title | Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism
of SUR2A-mediated cytoprotection independent from the K(ATP) channel
activity |
title_full | Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism
of SUR2A-mediated cytoprotection independent from the K(ATP) channel
activity |
title_fullStr | Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism
of SUR2A-mediated cytoprotection independent from the K(ATP) channel
activity |
title_full_unstemmed | Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism
of SUR2A-mediated cytoprotection independent from the K(ATP) channel
activity |
title_short | Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism
of SUR2A-mediated cytoprotection independent from the K(ATP) channel
activity |
title_sort | infection with av-sur2a protects h9c2 cells against metabolic stress: a mechanism
of sur2a-mediated cytoprotection independent from the k(atp) channel
activity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881534/ https://www.ncbi.nlm.nih.gov/pubmed/20123112 http://dx.doi.org/10.1016/j.bbamcr.2010.01.018 |
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