Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells

Kumar, Ashish; Sivanandam, Thamil Mani; Thakur, M. K.

doi:10.1515/tnsci-2016-0011

Cited by 7 publications

(5 citation statements)

References 32 publications

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“…Functional variants of PRKCB1 were identified to be associated with an increased likelihood of ASD (37). PSEN2 overexpression was observed to induce excessive apoptosis (17). Although the present study was unable to identify any association between the methylation of these genes and ASD, further studies with larger cohorts are required to clarify their roles in ASD.…”

Section: Discussionmentioning

confidence: 62%

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Association between the methylation of six apoptosis‑associated genes with autism spectrum disorder

Zhao

Zhou

et al. 2018

Mol Med Report

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Excessive apoptosis hinders the process of brain maturation and is regarded as one of the principal risk factors for the development of autism spectrum disorder (ASD). The aim of the present study was to investigate the association between the methylation of six apoptosis‑associated genes [transforming growth factor β 1 (TGFB1), BCL2 associated X, apoptosis regulator, insulin like growth factor binding protein 3, protein kinase C β 1, presenilin 2 and C‑C motif chemokine ligand 2] and ASD. Using quantitative methylation‑specific polymerase chain reaction technology, DNA methylation levels were detected in 42 autistic and 26 control subjects. The logistic regression analysis results demonstrated that of the six genes, only TGFB1 was significantly hypomethylated in peripheral blood samples from children with autism compared with control samples (mean percentage of methylated reference, 0.011% vs. 0.019%; age‑adjusted P=0.028). In addition, TGFB1 methylation was identified to be positively associated with the interaction ability score from the Autism Behavior Checklist (r=0.452; P=0.035). These data suggested that decreased TGFB1 methylation may contribute to the development of ASD.

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Section: Discussionmentioning

confidence: 62%

“…Protein kinase C β 1 (PRKCB1) was demonstrated to serve a pivotal role in ischemia/reperfusion-induced apoptosis (16). Presenilin 2 (PSEN2) overexpression was previously reported to be a cause of aberrant apoptosis (17).…”

Section: Introductionmentioning

confidence: 99%

Association between the methylation of six apoptosis‑associated genes with autism spectrum disorder

Zhao

Zhou

et al. 2018

Mol Med Report

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“…One important asset of our model is to overcome biases encountered by simple PSs overexpression . The major biases are abundant levels of inactive PSs and mislocalization of PSs in cells.…”

Section: Discussionmentioning

confidence: 99%

Specificity of presenilin‐1‐ and presenilin‐2‐dependent γ‐secretases towards substrate processing

Stanga

Vrancx

Tasiaux

et al. 2017

J Cellular Molecular Medi

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The two presenilin‐1 (PS1) and presenilin‐2 (PS2) homologs are the catalytic core of the γ‐secretase complex, which has a major role in cell fate decision and Alzheimer's disease (AD) progression. Understanding the precise contribution of PS1‐ and PS2‐dependent γ‐secretases to the production of β‐amyloid peptide (Aβ) from amyloid precursor protein (APP) remains an important challenge to design molecules efficiently modulating Aβ release without affecting the processing of other γ‐secretase substrates. To that end, we studied PS1‐ and PS2‐dependent substrate processing in murine cells lacking presenilins (PSs) (PS1KO, PS2KO or PS1‐PS2 double‐KO noted PSdKO) or stably re‐expressing human PS1 or PS2 in an endogenous PS‐null (PSdKO) background. We characterized the processing of APP and Notch on both endogenous and exogenous substrates, and we investigated the effect of pharmacological inhibitors targeting the PSs activity (DAPT and L‐685,458). We found that murine PS1 γ‐secretase plays a predominant role in APP and Notch processing when compared to murine PS2 γ‐secretase. The inhibitors blocked more efficiently murine PS2‐ than murine PS1‐dependent processing. Human PSs, especially human PS1, expression in a PS‐null background efficiently restored APP and Notch processing. Strikingly, and contrary to the results obtained on murine PSs, pharmacological inhibitors appear to preferentially target human PS1‐ than human PS2‐dependent γ‐secretase activity.

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“…PS1 can regulate the cell cycle through the Wnt/arm pathway and plays an important role in delaying cellular senescence and reducing oxidative stress [ 9 ]. PS2 overexpression is associated with apoptosis [ 10 ]. Synaptic dysfunction observed in a PS1 overexpressing Alzheimer’s disease cell model [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Muscle Psn gene combined with exercise contribute to healthy aging of skeletal muscle and lifespan by adaptively regulating Sirt1/PGC-1α and arm pathway

Gao,

Wen,

et al. 2024

PLoS ONE

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The Presenilin (Psn) gene is closely related to aging, but it is still unclear the role of Psn genes in skeletal muscle. Here, the Psn-UAS/Mhc-GAL4 system in Drosophila was used to regulate muscle Psn overexpression(MPO) and muscle Psn knockdown(MPK). Drosophila were subjected to endurance exercise from 4 weeks to 5 weeks old. The results showed that MPO and exercise significantly increased climbing speed, climbing endurance, lifespan, muscle SOD activity, Psn expression, Sirt1 expression, PGC-1α expression, and armadillo (arm) expression in aged Drosophila, and they significantly decreased muscle malondialdehyde levels. Interestingly, when the Psn gene is knockdown by 0.78 times, the PGC-1α expression and arm expression were also down-regulated, but the exercise capacity and lifespan were increased. Furthermore, exercise combined with MPO further improved the exercise capacity and lifespan. MPK combined with exercise further improves the exercise capacity and lifespan. Thus, current results confirmed that the muscle Psn gene was a vital gene that contributed to the healthy aging of skeletal muscle since whether it was overexpressed or knocked down, the aging progress of skeletal muscle structure and function was slowed down by regulating the activity homeostasis of Sirt1/PGC-1α pathway and Psn/arm pathway. Exercise enhanced the function of the Psn gene to delay skeletal muscle aging by up regulating the activity of the Sirt1/PGC-1α pathway and Psn/arm pathway.

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Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells

Cited by 7 publications

References 32 publications

Association between the methylation of six apoptosis‑associated genes with autism spectrum disorder

Association between the methylation of six apoptosis‑associated genes with autism spectrum disorder

Specificity of presenilin‐1‐ and presenilin‐2‐dependent γ‐secretases towards substrate processing

Muscle Psn gene combined with exercise contribute to healthy aging of skeletal muscle and lifespan by adaptively regulating Sirt1/PGC-1α and arm pathway

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