Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

Elaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation of NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome...

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Main Authors: Hui Liu, Xuenan Li, Ziyue Wang, Lu Li, Yucai Li, Haiyang Yan, Yuan Yuan
Format: Article
Language:English
Published: Tsinghua University Press 2024-01-01
Series:Food Science and Human Wellness
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Online Access:http://www.sciencedirect.com/science/article/pii/S2213453023001349
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author Hui Liu
Xuenan Li
Ziyue Wang
Lu Li
Yucai Li
Haiyang Yan
Yuan Yuan
author_facet Hui Liu
Xuenan Li
Ziyue Wang
Lu Li
Yucai Li
Haiyang Yan
Yuan Yuan
author_sort Hui Liu
collection DOAJ
description Elaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation of NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome, and sustained Ca2+ transfer can result in mitochondrial dysfunction. We focused on KCs to explore the damage to mitochondria by EA. After EA stimulation, cells produced an oxidative stress (OS) response with a significant increase in ROS release. Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca2+ led to Ca2+ accumulation in the mitochondrial matrix via mitochondria-associated membranes (MAMs). This was accompanied by a significant release of mROS, loss of MMP and ATP, and a significant increase in mitochondrial permeability transition pore opening, ultimately leading to mitochondrial instability. These findings confirmed the mechanism that EA induced mitochondrial Ca2+ imbalance in KCs via MAM, ultimately leading to mitochondrial dysfunction. Meanwhile, EA induced OS and the decrease of MMP and ATP in rat liver, and significant lesions were found in liver mitochondria. Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred, with a marked increase in lipid droplets.
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institution Kabale University
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publishDate 2024-01-01
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series Food Science and Human Wellness
spelling doaj-art-dbfcedbaf7114e40a1146d8b841cc1f52025-02-03T06:57:18ZengTsinghua University PressFood Science and Human Wellness2213-45302024-01-01131287298Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxesHui Liu0Xuenan Li1Ziyue Wang2Lu Li3Yucai Li4Haiyang Yan5Yuan Yuan6College of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCollege of Food Science and Engineering, Jilin University, Changchun 130062, ChinaCorresponding author at: College of Food Science and Engineering, Jilin University, Changchun 130062, China.; College of Food Science and Engineering, Jilin University, Changchun 130062, ChinaElaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation of NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome, and sustained Ca2+ transfer can result in mitochondrial dysfunction. We focused on KCs to explore the damage to mitochondria by EA. After EA stimulation, cells produced an oxidative stress (OS) response with a significant increase in ROS release. Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca2+ led to Ca2+ accumulation in the mitochondrial matrix via mitochondria-associated membranes (MAMs). This was accompanied by a significant release of mROS, loss of MMP and ATP, and a significant increase in mitochondrial permeability transition pore opening, ultimately leading to mitochondrial instability. These findings confirmed the mechanism that EA induced mitochondrial Ca2+ imbalance in KCs via MAM, ultimately leading to mitochondrial dysfunction. Meanwhile, EA induced OS and the decrease of MMP and ATP in rat liver, and significant lesions were found in liver mitochondria. Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred, with a marked increase in lipid droplets.http://www.sciencedirect.com/science/article/pii/S2213453023001349Elaidic acid (EA)Mitochondria-associated membranes (MAMs)CalciumEndoplasmic reticulumMitochondria dysfunction
spellingShingle Hui Liu
Xuenan Li
Ziyue Wang
Lu Li
Yucai Li
Haiyang Yan
Yuan Yuan
Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
Food Science and Human Wellness
Elaidic acid (EA)
Mitochondria-associated membranes (MAMs)
Calcium
Endoplasmic reticulum
Mitochondria dysfunction
title Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
title_full Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
title_fullStr Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
title_full_unstemmed Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
title_short Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes
title_sort elaidic acid leads to mitochondrial dysfunction via mitochondria associated membranes triggers disruption of mitochondrial calcium fluxes
topic Elaidic acid (EA)
Mitochondria-associated membranes (MAMs)
Calcium
Endoplasmic reticulum
Mitochondria dysfunction
url http://www.sciencedirect.com/science/article/pii/S2213453023001349
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