Cited by 50Alzheimer's disease research and treatmentsTraumatic Brain Injury and Neurovascular DisturbancesCell death mechanisms and regulation

Effects of ApoE on intracellular calcium levels and apoptosis of neurons after mechanical injury

Jiang, L., Zhong, J., Dou, X., Cheng, C., Huang, Z., Sun, X.·2015·Neuroscience

Abstract

Objective The current study aimed to explore the effects of apolipoprotein e (ApoE) on intracellular calcium ([Ca(2+)]i) and apoptosis of neurons after mechanical injury in vitro. Methods A neuron mechanical injury model was established after primary neurons obtained from APOE knockout and wild-type (WT) mice, and four experimental groups were generated: Group-ApoE4, Group-ApoE3, Group-ApoE(-) and Group-WT. Recombinant ApoE4 and ApoE3 were added to Group-ApoE4 and Group-ApoE3 respectively, and Group-ApoE(-) and Group-WT were control groups. Intracellular calcium was labeled by fluo-3/AM and examined using laser scanning confocal microscope and flow cytometry, and the apoptosis of neurons was also evaluated. Results The intracellular calcium levels and apoptosis rates of mice neurons were significantly higher in Group-ApoE4 than in Group-ApoE3 and Group-WT after mechanical injury. However, without mechanical injury on neurons, no significant differences in intracellular calcium levels and apoptosis rates were found among all four experimental groups. The effects of ApoE4 on intracellular calcium levels and apoptosis rates of injured neurons were partly decreased by EGTA treatment. Conclusion Compared with ApoE3-treatment and WT neurons, ApoE4 caused higher intracellular calcium levels and apoptosis rates of neurons after mechanical injury. This suggested APOE polymorphisms may affect neuron apoptosis after mechanical injury through different influences on intracellular calcium…

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Crossref · 10.1016/j.neuroscience.2015.06.005

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  • rhApoE3 reduced intracellular calcium levels in INV cells.

    “measurements of Ca2+ levels in INV cells showed that rhApoE3 reduced intracellular calcium levels (fig. S5P), in line with previous data (36).”

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Authors
Jiang, L., Zhong, J., Dou, X., Cheng, C., Huang, Z., & Sun, X.
Affiliations
  • The Affiliated Yongchuan Hospital of Chongqing Medical University (CN)
  • Chongqing Medical University (CN)
Venue
Neuroscience
Publisher
Elsevier BV
Published
2015-08
Volume
301
Pages
375-383
ISSN
0306-4522 (ISSN-L)
OpenAlex
W656703482
Cited by
50
References
6
Citations by year
2026: 1 · 2025: 4 · 2024: 3 · 2023: 3 · 2022: 6 · 2021: 10 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 2 · 2015: 1
FWCI
2.95
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
apolipoprotein E, APOE ε4, APOE3, intracellular calcium, neuronal apoptosis, mechanical damage, APOE polymorphism, EGTA, primary neurons, neuroprotection
MeSH terms
Analysis of Variance, Animals, Apolipoproteins E, Calcium, Cerebral Cortex, Flow Cytometry, Gene Expression Regulation, Intracellular Fluid, Neurons, Physical Stimulation, Stress, Mechanical, Time Factors, Apoptosis, Mice, Knockout, Mice, Apolipoprotein E3, Apolipoprotein E4

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