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Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons
Lipopolysaccharide (LPS), a fragment of the bacterial cell wall, specifically interacting with protein complexes on the cell surface, can induce the production of pro-inflammatory and apoptotic signaling molecules, leading to the damage and death of brain cells. Similar effects have been noted in st...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8767065/ https://www.ncbi.nlm.nih.gov/pubmed/35069113 http://dx.doi.org/10.3389/fnmol.2021.811171 |
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author | Bakaeva, Zanda Lizunova, Natalia Tarzhanov, Ivan Boyarkin, Dmitrii Petrichuk, Svetlana Pinelis, Vsevolod Fisenko, Andrey Tuzikov, Alexander Sharipov, Rinat Surin, Alexander |
author_facet | Bakaeva, Zanda Lizunova, Natalia Tarzhanov, Ivan Boyarkin, Dmitrii Petrichuk, Svetlana Pinelis, Vsevolod Fisenko, Andrey Tuzikov, Alexander Sharipov, Rinat Surin, Alexander |
author_sort | Bakaeva, Zanda |
collection | PubMed |
description | Lipopolysaccharide (LPS), a fragment of the bacterial cell wall, specifically interacting with protein complexes on the cell surface, can induce the production of pro-inflammatory and apoptotic signaling molecules, leading to the damage and death of brain cells. Similar effects have been noted in stroke and traumatic brain injury, when the leading factor of death is glutamate (Glu) excitotoxicity too. But being an amphiphilic molecule with a significant hydrophobic moiety and a large hydrophilic region, LPS can also non-specifically bind to the plasma membrane, altering its properties. In the present work, we studied the effect of LPS from Escherichia coli alone and in combination with the hyperstimulation of Glu-receptors on the functional state of mitochondria and Ca(2+) homeostasis, oxygen consumption and the cell survival in primary cultures from the rats brain cerebellum and cortex. In both types of cultures, LPS (0.1–10 μg/ml) did not change the intracellular free Ca(2+) concentration ([Ca(2+)](i)) in resting neurons but slowed down the median of the decrease in [Ca(2+)](i) on 14% and recovery of the mitochondrial potential (ΔΨm) after Glu removal. LPS did not affect the basal oxygen consumption rate (OCR) of cortical neurons; however, it did decrease the acute OCR during Glu and LPS coapplication. Evaluation of the cell culture survival using vital dyes and the MTT assay showed that LPS (10 μg/ml) and Glu (33 μM) reduced jointly and separately the proportion of live cortical neurons, but there was no synergism or additive action. LPS-effects was dependent on the type of culture, that may be related to both the properties of neurons and the different ratio between neurons and glial cells in cultures. The rapid manifestation of these effects may be the consequence of the direct effect of LPS on the rheological properties of the cell membrane. |
format | Online Article Text |
id | pubmed-8767065 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87670652022-01-20 Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons Bakaeva, Zanda Lizunova, Natalia Tarzhanov, Ivan Boyarkin, Dmitrii Petrichuk, Svetlana Pinelis, Vsevolod Fisenko, Andrey Tuzikov, Alexander Sharipov, Rinat Surin, Alexander Front Mol Neurosci Neuroscience Lipopolysaccharide (LPS), a fragment of the bacterial cell wall, specifically interacting with protein complexes on the cell surface, can induce the production of pro-inflammatory and apoptotic signaling molecules, leading to the damage and death of brain cells. Similar effects have been noted in stroke and traumatic brain injury, when the leading factor of death is glutamate (Glu) excitotoxicity too. But being an amphiphilic molecule with a significant hydrophobic moiety and a large hydrophilic region, LPS can also non-specifically bind to the plasma membrane, altering its properties. In the present work, we studied the effect of LPS from Escherichia coli alone and in combination with the hyperstimulation of Glu-receptors on the functional state of mitochondria and Ca(2+) homeostasis, oxygen consumption and the cell survival in primary cultures from the rats brain cerebellum and cortex. In both types of cultures, LPS (0.1–10 μg/ml) did not change the intracellular free Ca(2+) concentration ([Ca(2+)](i)) in resting neurons but slowed down the median of the decrease in [Ca(2+)](i) on 14% and recovery of the mitochondrial potential (ΔΨm) after Glu removal. LPS did not affect the basal oxygen consumption rate (OCR) of cortical neurons; however, it did decrease the acute OCR during Glu and LPS coapplication. Evaluation of the cell culture survival using vital dyes and the MTT assay showed that LPS (10 μg/ml) and Glu (33 μM) reduced jointly and separately the proportion of live cortical neurons, but there was no synergism or additive action. LPS-effects was dependent on the type of culture, that may be related to both the properties of neurons and the different ratio between neurons and glial cells in cultures. The rapid manifestation of these effects may be the consequence of the direct effect of LPS on the rheological properties of the cell membrane. Frontiers Media S.A. 2022-01-05 /pmc/articles/PMC8767065/ /pubmed/35069113 http://dx.doi.org/10.3389/fnmol.2021.811171 Text en Copyright © 2022 Bakaeva, Lizunova, Tarzhanov, Boyarkin, Petrichuk, Pinelis, Fisenko, Tuzikov, Sharipov and Surin. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Bakaeva, Zanda Lizunova, Natalia Tarzhanov, Ivan Boyarkin, Dmitrii Petrichuk, Svetlana Pinelis, Vsevolod Fisenko, Andrey Tuzikov, Alexander Sharipov, Rinat Surin, Alexander Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title | Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title_full | Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title_fullStr | Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title_full_unstemmed | Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title_short | Lipopolysaccharide From E. coli Increases Glutamate-Induced Disturbances of Calcium Homeostasis, the Functional State of Mitochondria, and the Death of Cultured Cortical Neurons |
title_sort | lipopolysaccharide from e. coli increases glutamate-induced disturbances of calcium homeostasis, the functional state of mitochondria, and the death of cultured cortical neurons |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8767065/ https://www.ncbi.nlm.nih.gov/pubmed/35069113 http://dx.doi.org/10.3389/fnmol.2021.811171 |
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