Cited by 83Multiple Sclerosis Research StudiesNeurogenesis and neuroplasticity mechanismsNeuroinflammation and Neurodegeneration Mechanisms

BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions

Kipp, M., Gingele, S., Pott, F., Clarner, T., van der Valk, P., Denecke, B., Gan, L., Siffrin, V. +7 more·2011·Brain, Behavior, and Immunity

Abstract

Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip® arrays. One finding was the predominance of immune and stress response factors in the group of genes which were classified as remyelination-supporting factors. We further demonstrate that lesions with impaired remyelination capacity show weak expression of the radial-glia cell marker brain lipid binding protein (BLBP, also called B-FABP or FABP7). The expression of BLBP in activated astrocytes correlates with the presence of oligodendrocyte progenitor cells. BLBP-expressing astrocytes are also detected in experimental autoimmune encephalomyelitis during the remission phase. Furthermore, highest numbers of BLBP-expressing astrocytes were evident in lesions of early MS, whereas significantly less are present at the rim of (chronic)-active lesions from patients with long disease duration. Transfection experiments show that BLBP regulates growth…

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Crossref · 10.1016/j.bbi.2011.05.003

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7 of 7 references verified0 citation errors · 0 not checkable

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  • Astrocytes show significantly lower gene and protein expression of GFAP after chronic demyelination compared to acute demyelination.

    “Since astrocytes show significantly lower gene and protein expression of GFAP after chronic demyelination compared to acute demyelination”
  • The activation status of astrocytes appears to be higher after acute demyelination than after chronic demyelination.

    “the activation status of astrocytes appears to be higher after acute demyelination (Ludwin, 1980; Kipp et al., 2011b)”
  • Under continuing cuprizone treatment, astrogliosis persists and after chronic demyelination the number of astrocytes is similar to acute demyelination.

    “Under continuing cuprizone treatment astrogliosis persists and after chronic demyelination the number of astrocytes is similar to acute demyelination (Lindner et al., 2009; Kipp et al., 2011b).”

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Authors
Kipp, M., Gingele, S., Pott, F., Clarner, T., van der Valk, P., Denecke, B., Gan, L., Siffrin, V., Zipp, F., Dreher, W., Baumgartner, W., Pfeifenbring, S., Godbout, R., Amor, S., & Beyer, C.
Affiliations
  • RWTH Aachen University (DE)
  • Johannes Gutenberg University Mainz (DE)
  • University of Bremen (DE)
  • Universitätsmedizin Göttingen (DE)
  • University of Alberta (CA)
  • Queen Mary University of London (GB)
Corresponding author
Kipp, M.
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2011-11
Volume
25
Issue
8
Pages
1554-1568
ISSN
0889-1591 (ISSN-L)
OpenAlex
W1994743569
Cited by
83
References
7
Citations by year
2026: 4 · 2025: 6 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 3 · 2019: 6 · 2018: 2 · 2017: 3 · 2016: 5 · 2015: 10 · 2014: 8 · 2013: 5 · 2012: 11
FWCI
6.28
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
  • Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
  • MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
  • GRO (submittedVersion)
  • RWTH Publications (RWTH Aachen) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
brain lipid-binding protein, FABP7, astrocytes, remyelination, multiple sclerosis, cuprizone, experimental autoimmune encephalomyelitis, oligodendrocyte precursor cells, demyelination, disease duration, gene expression, growth factor regulation, astrocyte activation
MeSH terms
Fatty Acid-Binding Protein 7, Adult, Aged, Animals, Astrocytes, Carrier Proteins, Cell Count, Cuprizone, Demyelinating Diseases, Encephalomyelitis, Autoimmune, Experimental, Female, Glial Fibrillary Acidic Protein, Humans, Immunohistochemistry, Male, Mice, Inbred C57BL, Middle Aged, Multiple Sclerosis, Nerve Tissue Proteins, Platelet-Derived Growth Factor, RNA, Messenger, Transfection, Blotting, Western, Fibroblast Growth Factor 2, Fluorescent Antibody Technique, Indirect, Oligonucleotide Array Sequence Analysis, Tumor Suppressor Proteins, Cell Line, Tumor, Fatty Acid-Binding Proteins, Mice, Osteopontin, Real-Time Polymerase Chain Reaction

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