Mutant presenilin 2 increased oxidative stress and p53 expression in neuronal cells

Nguyen, Huy Bang; Lee, Moon Soon; Hwang, Dae Youn; Kim, Young Kyu; Yoon, Do Young; Lee, Jae Woong; Yun, Yong Soo; Lee, Myung Koo; Oh, Ki Wan; Hong, Jin Tae

doi:10.1016/j.bbrc.2007.03.119

Cited by 19 publications

(12 citation statements)

References 32 publications

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“…Astrocytes are the source of released cytokine, which has been implicated in the amyloidogenesis during the development of AD [36]. So, we investigated the protective effect of EGCG against astrocyte activation.…”

Section: Effect Of Egcg On the Activation Of Astrocytes In The Lps-inmentioning

confidence: 99%

Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Lee

Choi

Yun

et al. 2013

The Journal of Nutritional Biochemistry

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175

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Section: Effect Of Egcg On the Activation Of Astrocytes In The Lps-inmentioning

confidence: 99%

Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Lee

Choi

Yun

et al. 2013

The Journal of Nutritional Biochemistry

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175

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“…(Pestov et al, 2001;Xu et al, 2001;Bender et al, 2002;Yuan et al, 2005;Nguyen et al, 2007). Mutations in these genes activate p53, leading to genomic instability, apoptosis, developmental atrophy of the brain, and other defects.…”

Section: Mutations In Cell-essential Genes Leading To P53 Upregulationmentioning

confidence: 99%

“…Mouse embryos deficient for bradykinin receptor B2 develop normally, but under saline stress, they develop a p53-mediated abnormal renal phenotype mimicking renal dysplasia in humans (Fan et al, 2006). Cells expressing mutant presenilin 2 function normally in the absence of oxidative stress, but respond to reactive oxygen species (ROS) by high p53 expres-sion (Nguyen et al, 2007), which may be involved in the neurodegeneration observed in Alzheimer's disease.…”

Section: Mutations In Cell-essential Genes Leading To P53 Upregulationmentioning

confidence: 99%

Role of p53 family in birth defects: Lessons from zebrafish

Danilova

Sakamoto

Lin

2008

Birth Defects Research Pt C

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p53 Protein family is an important teratologic suppressor, but in certain conditions it can cause congenital abnormalities. p53 Family performs this dual role in development by integrating information from cell's interior with that from the environment to determine the choice between life and death. Understanding of p53 family developmental functions may lead to new therapeutic approaches for treatment and prevention of birth defects. Zebrafish is becoming the vertebrate system of choice for studying p53 family role in development.

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“…There are contradictory reports showing the involvement of PS2 overexpression in apoptosis using different mammalian cell lines [18-20] as well as discrepancies in the underlying pathway. Some of the studies worth mentioning suggest that PS2 gene overexpression caused apoptosis [21], while its depletion protected against apoptotic cell death induced by trophic factor withdrawal or amyloid b (Ab) [22].…”

Section: Introductionmentioning

confidence: 99%

“…[23] showed that Bcl-X(L) interacts with PS1 and PS2 proteins, influencing mitochondrial-dependent apoptosis. Others considered that the activation of p53 signaling was the major effector contributing to PS2-induced apoptosis [24, 20]. These controversies prompted us to investigate whether PS2 overexpression causes apoptosis in mouse neuroblastoma (Neuro2a) cells and the underlying pathway.…”

Section: Introductionmentioning

confidence: 99%

Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells

Kumar

Sivanandam

Thakur

2016

Translational Neuroscience

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Presenilin 1 (PS1) and PS2 are evolutionarily conserved transmembrane proteins of the aspartyl protease family. Initially, they were reported to be associated with the early onset of familial, early-onset Alzheimer’s disease. PS1 has been implicated in several crucial brain functions including developmental processes, synaptic plasticity, and processing of various molecules, while PS2 has been poorly studied and is considered to be a compensatory partner of PS1. Certain controversial reports have suggested that PS2 has a role in apoptosis, though the underlying mechanism is not clear. To ascertain the role of PS2 in apoptosis, mouse neuroblastoma cells (Neuro2a) were transfected with a cDNA construct encoding full length mouse PS2 and analyzed for viability, expression of PS1, PS2, Bax and p53, Bax protein, and status of chromatin condensation. Our results showed reduced viability, condensed chromatin and higher expression of Bax at mRNA and protein levels, but no change in the expression of p53 and PS1 in PS2-overexpressing Neuro2a cells. Thus, it is evident that PS2, independent of PS1, is associated with apoptosis via a Bax-mediated pathway. These findings might help in the understanding of the involvement of PS2 in apoptosis and its associated brain disorders.

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Mutant presenilin 2 increased oxidative stress and p53 expression in neuronal cells

Cited by 19 publications

References 32 publications

Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Role of p53 family in birth defects: Lessons from zebrafish

Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells

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