b-series Ganglioside deficiency exhibits no definite changes in the neurogenesis and the sensitivity to Fas-mediated apoptosis but impairs regeneration of the lesioned hypoglossal nerve

Masahiko Okada, Michi Ichiro Itoh, Masashi Haraguchi, Tetsuya Okajima, Masahiro Inoue, Hideto Oishi, Yoichi Matsuda, Tsutomu Iwamoto, Toshihiro Kawano, Satoshi Fukumoto, Hiroshi Miyazaki, Keiko Furukawa, Shinichi Aizawa, Koichi Furukawa

Research output: Contribution to journalArticlepeer-review

148 Citations (Scopus)

Abstract

The polymorphic carbohydrate structures of gangliosides play regulatory roles. In particular, b-series gangliosides, all of which contain α-2,8 sialic acids, have been considered to be critical in various biological events such as adhesion, toxin binding, neurite extension, cell growth, and apoptosis. To clarify the physiological functions of b-series gangliosides in vivo, we have established a gene knockout mouse of GD3 synthase. Although all b-series structures were deleted in the mutant mice, they showed an almost complete nervous tissue morphology with no apparent abnormal behavior. Moreover, no differences in Fas-mediated apoptotic reaction of lymphocytes between wild type and the mutant mice were detected. However, the mutant mice exhibited clearly reduced regeneration of axotomized hypoglossal nerves compared with the wild type, suggesting that b-series gangliosides are more important in the repair rather than in the differentiation of the nervous system and apoptotic process induced via Fas.

Original languageEnglish
Pages (from-to)1633-1636
Number of pages4
JournalJournal of Biological Chemistry
Volume277
Issue number3
DOIs
Publication statusPublished - Jan 18 2002
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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