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Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells

Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present stu...

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Autores principales: Jin, Mei-Hua, Yu, Jia-Bin, Sun, Hu-Nan, Jin, Ying-Hua, Shen, Gui-Nan, Jin, Cheng-Hao, Cui, Yu-Dong, Lee, Dong-Seok, Kim, Sun-Uk, Kim, Ji-Su, Kwon, Taeho, Han, Ying-Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7023630/
https://www.ncbi.nlm.nih.gov/pubmed/31861323
http://dx.doi.org/10.3390/antiox9010001
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author Jin, Mei-Hua
Yu, Jia-Bin
Sun, Hu-Nan
Jin, Ying-Hua
Shen, Gui-Nan
Jin, Cheng-Hao
Cui, Yu-Dong
Lee, Dong-Seok
Kim, Sun-Uk
Kim, Ji-Su
Kwon, Taeho
Han, Ying-Hao
author_facet Jin, Mei-Hua
Yu, Jia-Bin
Sun, Hu-Nan
Jin, Ying-Hua
Shen, Gui-Nan
Jin, Cheng-Hao
Cui, Yu-Dong
Lee, Dong-Seok
Kim, Sun-Uk
Kim, Ji-Su
Kwon, Taeho
Han, Ying-Hao
author_sort Jin, Mei-Hua
collection PubMed
description Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present study, we observed significant increasing of intracellular ROS accumulations in Peroxiredoxin II (Prx II) knockdown HT22 cells, which were induced by alcohol treatments. We also found that the level of ROS in mitochondrial was also increased, resulting in a decrease in the mitochondrial membrane potential. The phosphorylation of GSK3β (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3β in Prx II knockdown HT22 cells. Moreover, NAC treatment also dramatically restored the mitochondrial membrane potential and the cellular apoptosis in Prx II knockdown HT22 cells. Our findings suggest that Prx II plays a crucial role in alcohol-induced neuronal cell apoptosis by regulating the cellular ROS levels, especially through regulating the ROS-dependent mitochondrial membrane potential. Consequently, Prx II may be a therapeutic target molecule for alcohol-induced neuronal cell death, which is closely related to ROS-dependent mitochondria dysfunction.
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spelling pubmed-70236302020-03-11 Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells Jin, Mei-Hua Yu, Jia-Bin Sun, Hu-Nan Jin, Ying-Hua Shen, Gui-Nan Jin, Cheng-Hao Cui, Yu-Dong Lee, Dong-Seok Kim, Sun-Uk Kim, Ji-Su Kwon, Taeho Han, Ying-Hao Antioxidants (Basel) Article Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present study, we observed significant increasing of intracellular ROS accumulations in Peroxiredoxin II (Prx II) knockdown HT22 cells, which were induced by alcohol treatments. We also found that the level of ROS in mitochondrial was also increased, resulting in a decrease in the mitochondrial membrane potential. The phosphorylation of GSK3β (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3β in Prx II knockdown HT22 cells. Moreover, NAC treatment also dramatically restored the mitochondrial membrane potential and the cellular apoptosis in Prx II knockdown HT22 cells. Our findings suggest that Prx II plays a crucial role in alcohol-induced neuronal cell apoptosis by regulating the cellular ROS levels, especially through regulating the ROS-dependent mitochondrial membrane potential. Consequently, Prx II may be a therapeutic target molecule for alcohol-induced neuronal cell death, which is closely related to ROS-dependent mitochondria dysfunction. MDPI 2019-12-18 /pmc/articles/PMC7023630/ /pubmed/31861323 http://dx.doi.org/10.3390/antiox9010001 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Jin, Mei-Hua
Yu, Jia-Bin
Sun, Hu-Nan
Jin, Ying-Hua
Shen, Gui-Nan
Jin, Cheng-Hao
Cui, Yu-Dong
Lee, Dong-Seok
Kim, Sun-Uk
Kim, Ji-Su
Kwon, Taeho
Han, Ying-Hao
Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title_full Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title_fullStr Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title_full_unstemmed Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title_short Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells
title_sort peroxiredoxin ii maintains the mitochondrial membrane potential against alcohol-induced apoptosis in ht22 cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7023630/
https://www.ncbi.nlm.nih.gov/pubmed/31861323
http://dx.doi.org/10.3390/antiox9010001
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