Cited by 179Neuroinflammation and Neurodegeneration MechanismsBiomarkers in Disease MechanismsCytokine Signaling Pathways and Interactions

Astrocyte and Macrophage Regulation of YKL‐40 Expression and Cellular Response in Neuroinflammation

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Bonneh‐Barkay, Dafna, Bissel, Stephanie J., Kofler, Julia, Starkey, Adam, Wang, Guoji, Wiley, Clayton A.·2012·Brain Pathology

Abstract

Numerous inflammatory conditions are associated with elevated YKL‐40 expression by infiltrating macrophages. Thus, we were surprised to observe minimal macrophage and abundant astrocyte expression of YKL‐40 in neuroinflammatory conditions. The aims of the current study were to better delineate this discrepancy, characterize the factors that regulate YKL‐40 expression in macrophages and astrocytes and study whether YKL‐40 expression correlates with cell morphology and/or activation state. In vitro, macrophages expressed high levels of YKL‐40 that was induced by classical activation and inhibited by alternative activation. Cytokines released from macrophages induced YKL‐40 transcription in astrocytes that was accompanied by morphological changes and altered astrocytic motility. Because coculturing of astrocytes and macrophages did not reverse this in vitro expression pattern, additional components of the in vivo central nervous system (CNS) milieu must be required to suppress macrophage and induce astrocyte expression of YKL‐40.

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Crossref · 10.1111/j.1750-3639.2011.00550.x

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  • YKL-40 is mainly expressed by astrocytes, but also by microglia, often in close vicinity to senile plaques and neurofibrillary tangles.

    “YKL-40 is mainly expressed by astrocytes, but also by microglia, often in close vicinity to senile plaques and neurofibrillary tangles [15–17].”

    From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [17]

    The Results section reports YKL-40 expression in reactive astrocytes in the examined neuroinflammatory conditions, supporting the astrocyte portion of the claim. It reports no YKL-40 staining in the examined parenchymal microglia, and does not address proximity to senile plaques or neurofibrillary tangles. No page numbers are available in our copy. (LLM, conf=0.88)

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Cited by

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Authors
Bonneh‐Barkay, D., Bissel, S. J., Kofler, J., Starkey, A., Wang, G., & Wiley, C. A.
Affiliations
University of Pittsburgh (US)
Venue
Brain Pathology
Publisher
Wiley
Published
2011-12-22
Volume
22
Issue
4
Pages
530-546
ISSN
  • 1015-6305 (ISSN-L)
  • 1750-3639
OpenAlex
W1585095351
Cited by
179
References
1
Citations by year
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FWCI
1.58
Type
journal article
Language
en
Open access
Locations
  • Brain Pathology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Medical Center, University of Pittsburgh
  • National Institute on Aging (R21AG025829)
  • National Institute of Mental Health (K24MH001717, R01MH071151)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
YKL-40, astrocytes, macrophages, neuroinflammation, macrophage polarization, classical activation, alternative activation, cytokines, astrocyte morphology, gene expression regulation, central nervous system
MeSH terms
Chitinase-3-Like Protein 1, Astrocytes, Brain, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Fluorescent Antibody Technique, Humans, Inflammation, Macrophages, Blotting, Western, In Situ Hybridization, Coculture Techniques, Lectins, Adipokines, Real-Time Polymerase Chain Reaction

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