Cited by 14Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsPluripotent Stem Cells Research

APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes

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de Leeuw, Sherida M., Kirschner, Aron W.T., Lindner, Karina, Rust, Ruslan, Budny, Vanessa, Wolski, Witold E., Gavin, Anne-Claude, Nitsch, Roger M. +1 more·2022·Stem Cell Reports

Abstract

(Stem Cell Reports 17, 110–126; January 11, 2022) In the initial version of this article, there was an error in the merged image for APOE3 in Figure 1E. While all individual images for S100β and GJA1 were displayed correctly, we accidentally merged APOE3 GJA1 with APOE2 S100β (and not with the S100β image of APOE3). However, this error did not affect the figure’s meaning or conclusion. The correct merged GJA1/S100β staining for APOE3 iAstrocytes has now been included in the article online and below. No correction of the text or figure legend was necessary.Figure 1. APOE-isogenic iPSCs are differentiated to iAstrocytes (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT) APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytesde Leeuw et al.Stem Cell ReportsDecember 16, 2021In BriefIn this article, Tackenberg and colleagues show APOE genotype-dependent differences in the proteomic profile of APOE-isogenic iPSC-derived human astrocytes. They provide evidence for a pro-inflammatory state of APOE4 iAstrocytes, while APOE2 and APOE-KO iAstrocytes show reduced inflammatory signaling. They further show the APOE genotype-dependent regulation of β-amyloid uptake capacity and cholesterol/lipid homeostasis and a differential reaction to inflammatory stimuli. Full-Text PDF Open Access

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Crossref · 10.1016/j.stemcr.2022.03.018

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  • In vitro studies show APOE genetic variation can alter cellular metabolic profiles in distinct cell types including astrocytes, microglia, and neurons.

    “Studies performed in vitro have shown that APOE genetic variation can alter cellular metabolic profiles in distinct cell types including astrocytes, microglia, and neurons [27][28][29][30] .”

    From APOE4-drives brain bioenergetic shifts independent of Alzheimer’s disease pathology (2026) · cites this paper as [27]

    Our copy contains only a correction notice (pp. 1229–1231), not the study’s findings. It identifies APOE-isogenic iPSC-derived astrocytes, but does not establish the claimed changes in metabolic profiles or address microglia and neurons. The original article’s results may be missing from our copy. (LLM, conf=0.73)

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Authors
de Leeuw, S. M., Kirschner, A. W. T., Lindner, K., Rust, R., Budny, V., Wolski, W. E., Gavin, A.-C., Nitsch, R. M., & Tackenberg, C.
Affiliations
University of Zurich (CH)
Corresponding author
Tackenberg, Christian
Venue
Stem Cell Reports
Publisher
Elsevier BV
Published
2022-05
Volume
17
Issue
5
Pages
1229-1231
ISSN
2213-6711 (ISSN-L)
OpenAlex
W4280539972
Cited by
14
References
0
Citations by year
2026: 5 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 1
FWCI
0.78
Type
journal article
Language
en
Open access
Locations
  • Stem Cell Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by)
  • Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
  • ETH Zürich Research Collection
  • Zurich Open Repository and Archive (University of Zurich)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Keywords
APOE2, APOE3, APOE ε4, APOE genotype, cholesterol metabolism, lipid homeostasis, inflammation, proteomic profiling, S100β, connexin 43, Alzheimer's disease

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