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タイトル
  • Semaphorin 3A Binds to the Perineuronal Nets via Chondroitin Sulfate Type E Motifs in Rodent Brains
作成者

Dick, Gunnar

Tan, Chin Lik

Alves, Joao Nuno

Ehlert, Erich M. E.

Miller, Gregory M.

Hsieh-Wilson, Linda C.

Sugahara, Kazuyuki

Oosterhof, Arie

van Kuppevelt, Toin H.

Verhaagen, Joost

Fawcett, James W.

Kwok, Jessica C. F.

権利情報
    • This research was originally published in Journal of Biological Chemistry. Gunnar Dick, Chin Lik Tan, Joao Nuno Alves, Erich M. E. Ehlert, Gregory M. Miller, Linda C. Hsieh-Wilson,Kazuyuki Sugahara, Arie Oosterhof, Toin H. van Kuppevelt, Joost Verhaagen, James W. Fawcett,and Jessica C. F. Kwok. Semaphorin 3A Binds to the Perineuronal Nets viaChondroitin Sulfate Type E Motifs in Rodent Brains. Journal of Biological Chemistry. 2013; Vol:288(38) p27384–27395. © the American Society for Biochemistry and Molecular Biology
主題
  • Other Chondroitin Sulfate
  • Other Glycosaminoglycan
  • Other Proteoglycan
  • Other Regeneration
  • Other Semaphorin
  • Other Semaphorin3A
  • Other Neuronal Plasticity
  • Other Perineuronal nets
  • NDC 460
内容注記
Other
  • Chondroitin sulfate (CS) and the CS-rich extracellular matrix structures called perineuronal nets (PNNs) restrict plasticity and regeneration in the CNS. Plasticity is enhanced by chondroitinase ABC treatment that removes CS from its core protein in the chondroitin sulfate proteoglycans or by preventing the formation of PNNs, suggesting that chondroitin sulfate proteoglycans in the PNNs control plasticity. Recently, we have shown that semaphorin3A (Sema3A), a repulsive axon guidance molecule, localizes to the PNNs and is removed by chondroitinase ABC treatment (Vo, T., Carulli, D., Ehlert, E. M., Kwok, J. C., Dick, G., Mecollari, V., Moloney, E. B., Neufeld, G., de Winter, F., Fawcett, J. W., and Verhaagen, J. (2013) Mol. Cell. Neurosci. 56C, 186–200). Sema3A is therefore a candidate for a PNN effector in controlling plasticity. Here, we characterize the interaction of Sema3A with CS of the PNNs. Recombinant Sema3A interacts with CS type E (CS-E), and this interaction is involved in the binding of Sema3A to rat brain-derived PNN glycosaminoglycans, as demonstrated by the use of CS-E blocking antibody GD3G7. In addition, we investigate the release of endogenous Sema3A from rat brain by biochemical and enzymatic extractions. Our results confirm the interaction of Sema3A with CS-E containing glycosaminoglycans in the dense extracellular matrix of rat brain. We also demonstrate that the combination of Sema3A and PNN GAGs is a potent inhibitor of axon growth, and this inhibition is reduced by the CS-E blocking antibody. In conclusion, Sema3A binding to CS-E in the PNNs may be a mechanism whereby PNNs restrict growth and plasticity and may represent a possible point of intervention to facilitate neuronal plasticity.
出版者American Society for Biochemistry and Molecular Biology (ASBMB)
日付 Issued 2013-09-20
言語eng
資源タイプjournal article
出版タイプVoR
資源識別子 URI http://hdl.handle.net/2115/62910
関連
  • isIdenticalTo PMID 23940048
  • isIdenticalTo DOI https://doi.org/10.1074/jbc.M111.310029
収録誌情報
    • ISSN 0021-9258
    • ISSN 1083-351X
    • Journal of Biological Chemistry
    288(38), 27384-27395
ファイル
コンテンツ更新日時2019-10-09T00:14:31Z