論文

国際誌
2020年10月20日

Deletion of CD38 and supplementation of NAD+ attenuate axon degeneration in a mouse facial nerve axotomy model.

Scientific reports
  • Yuji Takaso
  • ,
  • Masao Noda
  • ,
  • Tsuyoshi Hattori
  • ,
  • Jureepon Roboon
  • ,
  • Miyako Hatano
  • ,
  • Hisashi Sugimoto
  • ,
  • Charles Brenner
  • ,
  • Yasuhiko Yamamoto
  • ,
  • Hiroshi Okamoto
  • ,
  • Haruhiro Higashida
  • ,
  • Makoto Ito
  • ,
  • Tomokazu Yoshizaki
  • ,
  • Osamu Hori

10
1
開始ページ
17795
終了ページ
17795
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-020-73984-3

Following facial nerve axotomy, nerve function is not fully restored even after reconstruction. This may be attributed to axon degeneration/neuronal death and sustained neuroinflammation. CD38 is an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD+) and is a candidate molecule for regulating neurodegeneration and neuroinflammation. In this study, we analyzed the effect of CD38 deletion and NAD+ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice. Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different. In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy. Supplementation of NAD+ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy. These results suggest that CD38 deletion and supplementation of NAD+ may protect transected axon cell-autonomously after facial nerve axotomy.

リンク情報
DOI
https://doi.org/10.1038/s41598-020-73984-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/33082370
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576594
ID情報
  • DOI : 10.1038/s41598-020-73984-3
  • PubMed ID : 33082370
  • PubMed Central 記事ID : PMC7576594

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