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

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13 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)93-103
Number of pages11
JournalBiological Trace Element Research
Volume113
Issue number1
DOIs
Publication statusPublished - 2006 Oct

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Keywords

  • Amyotrophic lateral sclerosis
  • Kidney
  • Liver
  • Metallothionein-I
  • Metallothionein-III
  • Rodent model
  • Spinal cord

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Clinical Biochemistry
  • Biochemistry, medical
  • Inorganic Chemistry

Cite this

Ono, S. I., Endo, Y., Tokuda, E. I., Ishige, K., Tabata, K. I., Asami, S., Ito, Y., & Suzuki, T. (2006). Upregulation of metallothionein-I mRNA expression in a rodent model for amyotrophic lateral sclerosis. Biological Trace Element Research, 113(1), 93-103. https://doi.org/10.1385/BTER:113:1:93