Increased syndecan expression by pleiotrophin and FGF receptor‐expressing astrocytes in injured brain tissue
Abstract
Syndecan-1, -2, -3, and -4 are heparan sulfate proteoglycans that are differentially expressed during development and wound repair. To determine whether syndecans are also involved in brain injury, we examined the expression of syndecan core proteins genes in cryo-injured mouse brain, using in situ hybridization. All syndecan mRNA transcripts were similarly expressed in the region surrounding the necrotic tissue, exhibiting peak levels at day 7 after injury. Comparison with cellular markers showed that reactive astrocytes were the primary source of syndecans. Syndecans serve as co-receptors for fibroblast growth factor (FGF) and as a reservoir for another heparin-binding growth factor, pleiotrophin (PTN, or heparin-binding growth-associated molecule. In our model, FGF receptor1 (FGFR1) and PTN mRNA levels were upregulated in reactive astrocytes. The distribution patterns of FGFR1 and PTN overlapped considerably with those of syndecan-1 and -3 mRNAs, respectively. These results suggest that syndecans are expressed primarily in reactive astrocytes, and may provide a supportive environment for regenerating axons in concert with heparin-binding growth factors (e.g., FGF and PTN) in the injured brain.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Astrocyte-derived PTN is an anti-inflammatory, neuroprotective factor secreted by reactive astrocytes.
“Accumulating evidence points to astrocyte‐derived PTN as an anti‐inflammatory, neuroprotective factor secreted by reactive astrocytes. 43 , 44”
From Loss of <i>Inpp5d</i> has disease‐relevant and sex‐specific effects on glial transcriptomes (2024) · cites this paper as [44]
Cites
Microglia-specific localisation of a novel calcium binding protein, Iba1
Ito, D., Imai, Y., Ohsawa, K., Nakajima, K., Fukuuchi, Y., & Kohsaka, S. (1998) · Molecular Brain Research · doi:10.1016/s0169-328x(98)00040-0 · Cited by 1,476 · see citing works
Imai, Y., Ibata, I., Ito, D., Ohsawa, K., & Kohsaka, S. (1996) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1996.1112 · Cited by 872 · see citing works
Kinnunen, T., Raulo, E., Nolo, R., Maccarana, M., Lindahl, U., & Rauvala, H. (1996) · Journal of Biological Chemistry · doi:10.1074/jbc.271.4.2243 · Cited by 127 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Snow, A. D., Cummings, J. A., & Lake, T. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.710683 · Cited by 84 · see citing works
The midkine family of growth factors: diverse roles in nervous system formation and maintenance
Winkler, C., & Yao, S. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12462 · Cited by 72 · see citing works
Acute Brain Injury Triggers MyD88-Dependent, TLR2/4-Independent Inflammatory Responses
Koedel, U., Merbt, U. M., Schmidt, C., Angele, B., Popp, B., Wagner, H., Pfister, H.-W., & Kirschning, C. J. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.060821 · Cited by 78 · see citing works
Loss of <i>Inpp5d</i> has disease‐relevant and sex‐specific effects on glial transcriptomes
Dabin, L. C., Kersey, H., Kim, B., Acri, D. J., Sharify, D., Lee‐Gosselin, A., Lasagna‐Reeves, C. A., Oblak, A. L., Lamb, B. T., & Kim, J. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13901 · Cited by 10 · see citing works
“43,44 Downregulation of this signaling pathway through the loss of Inpp5d could, therefore, enhance neuroinflammation.”
- Authors
- Iseki, K., Hagino, S., Mori, T., Zhang, Y., Yokoya, S., Takaki, H., Tase, C., Murakawa, M., & Wanaka, A.
- Affiliations
- Fukushima Medical University (JP)
- Corresponding author
- Iseki, Ken
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2002-05-13
- Volume
- 39
- Issue
- 1
- Pages
- 1-9
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2158859972
- Cited by
- 78
- References
- 3
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 8 · 2013: 6 · 2012: 2
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Keywords
- syndecans, pleiotrophin, FGF receptor 1, reactive astrocytes, brain injury, heparan sulfate proteoglycans, heparin-binding growth factors, axon regeneration, necrotic tissue, gene expression
- MeSH terms
- Animals, Astrocytes, Brain Injuries, Carrier Proteins, Male, Membrane Glycoproteins, Mice, Inbred ICR, Proteoglycans, RNA, Messenger, Up-Regulation, Cytokines, Receptors, Fibroblast Growth Factor, Receptor Protein-Tyrosine Kinases, Mice, Receptor, Fibroblast Growth Factor, Type 1, Syndecans, Syndecan-1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
