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Increased syndecan expression by pleiotrophin and FGF receptor‐expressing astrocytes in injured brain tissue
Author(s) -
Iseki Ken,
Hagino Seita,
Mori Tetsuji,
Zhang Yuxiang,
Yokoya Sachihiko,
Takaki Hiromi,
Tase Choichiro,
Murakawa Masahiro,
Wanaka Akio
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10078
Subject(s) - pleiotrophin , syndecan 1 , fibroblast growth factor , biology , in situ hybridization , microbiology and biotechnology , growth factor , heparan sulfate , receptor , fibroblast growth factor receptor , astrocyte , fibroblast growth factor receptor 1 , basic fibroblast growth factor , gene expression , gene , heparin , central nervous system , neuroscience , cell , genetics , biochemistry
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. GLIA 39:1–9, 2002. © 2002 Wiley‐Liss, Inc.