Paired immunoglobulin-like receptor B knockout does not enhance axonal regeneration or locomotor recovery after spinal cord injury

Yuka Nakamura, Yuki Fujita, Masaki Ueno, Toshiyuki Takai, Toshihide Yamashita

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Myelin components that inhibit axonal regeneration are believed to contribute significantly to the lack of axonal regeneration noted in the adult central nervous system. Three proteins found in myelin, Nogo, myelin-associated glycoprotein, and oligodendrocyte-myelin glycoprotein, inhibit neurite outgrowth in vitro. All of these proteins interact with the same receptors, namely, the Nogo receptor (NgR) and paired immunoglobulin- like receptor B (PIR-B). As per previous reports, corticospinal tract (CST) regeneration is not enhanced in NgRknock- out mice after spinal cord injury. Therefore, we assessed CST regeneration in PIR-B-knock-out mice. We found that hindlimb motor function, as assessed using the Basso mouse scale, footprint test, inclined plane test, and beam walking test, did not differ between the PIR-B-knock-out and wildtype mice after dorsal hemisection of the spinal cord. Further, tracing of the CST fibers after injury did not reveal enhanced axonal regeneration or sprouting in the CST of the PIR-Bknock- out mice. Systemic administration of NEP1-40, a NgR antagonist, to PIR-B knock-out mice did not enhance the regenerative response. These results indicate that PIR-B knockout is not sufficient to induce extensive axonal regeneration after spinal cord injury.

Original languageEnglish
Pages (from-to)1876-1883
Number of pages8
JournalJournal of Biological Chemistry
Volume286
Issue number3
DOIs
Publication statusPublished - 2011 Jan 21

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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