Antiproliferative Role of Secondary Metabolites From Aspergillus unguis AG 1.1 (G) Isolated From Marine Macroalgae Enteromorpha sp. by Inducing Intracellular ROS Production and Mitochondrial Membrane Potential Loss Leading to Apoptosis

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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Aquaporin3 expression and the potential role of aquaporins in motility and mitochondrial membrane potential in human spermatozoa

Andrologia ◽

10.1111/and.13588 ◽

2020 ◽

Vol 52 (6) ◽

Author(s):

Atieh Alyasin ◽

Hamid Reza Momeni ◽

Majid Mahdieh

Keyword(s):

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Potential Role ◽

Human Spermatozoa

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The Short Isoform of DNAJB6 Protects against 1-Methyl-4-phenylpridinium Ion-Induced Apoptosis in LN18 Cells via Inhibiting Both ROS Formation and Mitochondrial Membrane Potential Loss

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/7982389 ◽

2017 ◽

Vol 2017 ◽

pp. 1-12 ◽

Cited By ~ 1

Author(s):

Yeon-Mi Hong ◽

Yohan Hong ◽

Yeong-Gon Choi ◽

Sujung Yeo ◽

Soo Hee Jin ◽

...

Keyword(s):

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Molecular Mechanisms ◽

Mitochondrial Pathway ◽

Caspase 9 ◽

Ros Formation ◽

Mitochondrial Membrane Potential Loss ◽

Induced Apoptosis ◽

Shock Proteins

In a previous study, we found that the short isoform of DNAJB6 (DNAJB6(S)) had been decreased in the striatum of a mouse model of Parkinson’s disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). DNAJB6, one of the heat shock proteins, has been implicated in the pathogenesis of PD. In this study, we explored the cytoprotective effect of DNAJB6(S) against 1-methyl-4-phenylpyridinium ion- (MPP+-) induced apoptosis and the underlying molecular mechanisms in cultured LN18 cells from astrocytic tumors. We observed that MPP+ significantly reduced the cell viability and induced apoptosis in LN18 glioblastoma cells. DNAJB6(S) protected LN18 cells against MPP+-induced apoptosis not only by suppressing Bax cleavage but also by inhibiting a series of apoptotic events including loss of mitochondrial membrane potential, increase in intracellular reactive oxygen species, and activation of caspase-9. These observations suggest that the cytoprotective effects of DNAJB6(S) may be mediated, at least in part, by the mitochondrial pathway of apoptosis.

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Involvement of Hydrogen Peroxide in the Manganese-Induced Myocytes Mitochondrial Membrane Potential Loss

Toxicology Mechanisms and Methods ◽

10.1080/15376510802428583 ◽

2008 ◽

Vol 19 (1) ◽

pp. 66-72 ◽

Cited By ~ 2

Author(s):

Huijuan Yang ◽

Ling Gu ◽

Le Zhang ◽

Ming Yan ◽

Xiaoxiang Zheng

Keyword(s):

Hydrogen Peroxide ◽

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Potential Loss ◽

Mitochondrial Membrane Potential Loss

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Rhomboid Protease PARL Mediates the Mitochondrial Membrane Potential Loss-induced Cleavage of PGAM5

Journal of Biological Chemistry ◽

10.1074/jbc.m112.357509 ◽

2012 ◽

Vol 287 (41) ◽

pp. 34635-34645 ◽

Cited By ~ 87

Author(s):

Shiori Sekine ◽

Yusuke Kanamaru ◽

Masato Koike ◽

Ayako Nishihara ◽

Masahiro Okada ◽

...

Keyword(s):

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Rhomboid Protease ◽

Potential Loss ◽

Mitochondrial Membrane Potential Loss

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The Interferon Stimulator Mitochondrial Antiviral Signaling Protein Facilitates Cell Death by Disrupting the Mitochondrial Membrane Potential and by Activating Caspases

Journal of Virology ◽

10.1128/jvi.02174-09 ◽

2009 ◽

Vol 84 (5) ◽

pp. 2421-2431 ◽

Cited By ~ 41

Author(s):

Chia-Yi Yu ◽

Ruei-Lin Chiang ◽

Tsung-Hsien Chang ◽

Ching-Len Liao ◽

Yi-Ling Lin

Keyword(s):

Cell Death ◽

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Caspase Cleavage ◽

Infected Cells ◽

Mitochondrial Antiviral Signaling ◽

Antiviral Innate Immunity ◽

Viral Components

ABSTRACT Interferon (IFN) signaling is initiated by the recognition of viral components by host pattern recognition receptors. Dengue virus (DEN) triggers IFN-β induction through a molecular mechanism involving the cellular RIG-I/MAVS signaling pathway. Here we report that the MAVS protein level is reduced in DEN-infected cells and that caspase-1 and caspase-3 cleave MAVS at residue D429. In addition to its well-known function in IFN induction, MAVS is also a proapoptotic molecule that triggers disruption of the mitochondrial membrane potential and activation of caspases. Although different domains are required for the induction of cytotoxicity and IFN, caspase cleavage at residue 429 abolished both functions of MAVS. The apoptotic role of MAVS in viral infection and double-stranded RNA (dsRNA) stimulation was demonstrated in cells with reduced endogenous MAVS expression induced by RNA interference. Even though IFN-β promoter activation was largely suppressed, DEN production was not affected greatly in MAVS knockdown cells. Instead, DEN- and dsRNA-induced cell death and caspase activation were delayed and attenuated in the cells with reduced levels of MAVS. These results reveal a new role of MAVS in the regulation of cell death beyond its well-known function of IFN induction in antiviral innate immunity.

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