Upregulation of metallothionein-I mRNA expression in a rodent model for amyotrophic lateral sclerosis

Shin Ichi Ono, Yuko Endo, Ei Ichi Tokuda, Kumiko Ishige, Kei Ichi Tabata, Satoru Asami, Yoshihisa Ito, Takashi Suzuki

研究成果: Article査読

14 被引用数 (Scopus)

抄録

Metallothionein (MT) mRNA expression was investigated in a rodent model (G93A SOD1 transgenic mouse) for a lethal motor neuron disease, amyotrophic lateral sclerosis (ALS). In 8-wk-old mice that did not yet exhibit motor paralysis, MT-I mRNA expression was already significantly upregulated in the region of the spinal cord responsible for motor paralysis. The expression of another isoform, MT-III, was not changed. In the cerebellum, which is not responsible for motor paralysis in ALS, neither the expression profiles of MT-I nor MT-III were altered. In 16-wk-old mice exhibiting motor paralysis, the expression of MT-I mRNA remained upregulated and the MT-III level tended to be elevated. Although no significant differences were found in the levels of both isoforms in the liver or kidney of 8-wk-old mice, the MT-I mRNA expression level was significantly upregulated in the kidney and liver of 16-wk-old mice. These results indicated that the MT-I isoform, but not the MT-III isoform, is associated with motor neuron death in ALS and suggested that the disease might be a systemic disorder to which the spinal cord is particularly susceptible.

本文言語English
ページ(範囲)93-103
ページ数11
ジャーナルBiological Trace Element Research
113
1
DOI
出版ステータスPublished - 2006 10月

ASJC Scopus subject areas

  • 内分泌学、糖尿病および代謝内科学
  • 生化学
  • 臨床生化学
  • 生化学、医学
  • 無機化学

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