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Endothelial-Ercc1 DNA repair deficiency provokes blood-brain barrier dysfunction

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Hansen, Cathrin E., Vacondio, Davide, van der Molen, Lennart, Jüttner, Annika A., Fung, Wing Ka, Karsten, Manon, van het Hof, Bert, Fontijn, Ruud D. +6 more·2025·Cell Death & Disease
DOI 10.1038/s41419-024-07306-0PMC PMC11698980

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Abstract

Aging of the brain vasculature plays a key role in the development of neurovascular and neurodegenerative diseases, thereby contributing to cognitive impairment. Among other factors, DNA damage strongly promotes cellular aging, however, the role of genomic instability in brain endothelial cells (EC) and its potential effect on brain homeostasis is still largely unclear. We here investigated how endothelial aging impacts blood-brain barrier (BBB) function by using excision repair cross complementation group 1 (ERCC1)-deficient human brain ECs and an EC-specific Ercc1 knock out (EC-KO) mouse model. In vitro, ERCC1-deficient brain ECs displayed increased senescence-associated secretory phenotype expression, reduced BBB integrity, and higher sprouting capacities due to an underlying dysregulation of the Dll4-Notch pathway. In line, EC-KO mice showed more P21 + cells, augmented expression of angiogenic markers, and a concomitant increase in the number of brain ECs and pericytes. Moreover, EC-KO mice displayed BBB leakage and enhanced cell adhesion molecule expression accompanied by peripheral immune cell infiltration into the brain. These findings were confined to the white matter, suggesting a regional susceptibility. Collectively, our results underline the role of endothelial aging as a driver of impaired BBB function, endothelial sprouting, and increased immune cell migration into the brain, thereby contributing to impaired brain homeostasis as observed during the aging process.

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  • Dysfunction of SHIP1 has been associated with a spectrum of diseases, including AD, AML, SLE, RA.

    “As such, dysfunction of SHIP1 has been associated with a spectrum of diseases, including Alzheimer’s disease (AD), acute myeloid leukemia (AML) and autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA)3–6.”

    From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [6]

    The Results section on ERCC1 deficiency and blood-brain barrier impairment concerns ERCC1, not SHIP1. Searches of our copy for SHIP1, INPP5D, acute myeloid leukemia, lupus, and rheumatoid arthritis found no passage linking SHIP1 dysfunction to the listed diseases. The paper mentions Alzheimer’s disease in another context, without making the claimed SHIP1 association. (LLM, conf=0.77)

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Cited by

Sorted by citations

Authors
Hansen, C. E., Vacondio, D., van der Molen, L., Jüttner, A. A., Fung, W. K., Karsten, M., van het Hof, B., Fontijn, R. D., Kooij, G., Witte, M. E., Roks, A. J. M., de Vries, H. E., Mulder, I., & de Wit, N. M.
Affiliations
  • Amsterdam Neuroscience (NL)
  • Erasmus MC (NL)
  • Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
  • Amsterdam UMC Location University of Amsterdam (NL)
Corresponding author
Hansen, Cathrin E.
ORCID
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2025-01-03
Volume
16
Issue
1
Pages
1-1
ISSN
2041-4889 (ISSN-L)
DOI
10.1038/s41419-024-07306-0
PMC
PMC11698980
OpenAlex
W4406026710
Cited by
27
References
16
Citations by year
2026: 16 · 2025: 11
FWCI
9.74
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Death and Disease (publishedVersion, cc-by)
  • Research Square (acceptedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, cc-by)
  • Pure Amsterdam UMC (submittedVersion, cc-by)
  • Radboud Repository (Radboud University) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • European Commission (813294, HORIZON2020, 101097983)
  • ZonMw (10510022110005)
  • Nederlandse Organisatie voor Wetenschappelijk Onderzoek (91719305)
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Keywords
ERCC1, DNA repair deficiency, brain endothelial cells, endothelial aging, blood-brain barrier dysfunction, genomic instability, senescence-associated secretory phenotype, Dll4-Notch signaling, angiogenesis, pericytes, immune cell infiltration, white matter, brain aging, neurodegenerative diseases
MeSH terms
Animals, Blood-Brain Barrier, Brain, DNA Repair, DNA-Binding Proteins, Endonucleases, Humans, Mice, Inbred C57BL, Cellular Senescence, Mice, Knockout, Endothelial Cells, Mice

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