Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene

M. Shiote, H. Ilieva, I. Nagano, T. Murakami, T. Hayashi, M. Shoji, K. Abe

Research output: Contribution to journalArticle

Abstract

We examined expressions of phosphatidylinositol 3-kinase (PI3-K), Akt and redox factor-1 protein (Ref-1) in the spinal cord of transgenic mice with G93A mutant superoxide dismutase (SOD1) (Tg), a valuable model of human amyotrophic lateral sclerosis (ALS), at early and presymptomatic stage, 18 and 25 weeks of age. Significant decrease of PI3-K, and Akt in Tg/18 mice, and of PI3-K, Akt and Ref-1 in Tg/25 was observed on immunoblotting. Immunohistochemistry revealed the significant decrease of PI3-K, Akt and Ref-1 in spinal motor neurons of Tg/25 mice. No significant loss of anterior horn neurons was detected. Therefore, the decrease of survival signal or impairment of DNA repair in the spinal motor neurons precedes a subsequent death of anterior horn neurons, and may account for the mutant SOD1-mediated motor neuronal death in this model.

Original languageEnglish
Pages (from-to)65-71
Number of pages7
JournalInternational Congress Series
Volume1252
Issue numberC
DOIs
Publication statusPublished - Jun 1 2003

Fingerprint

Phosphatidylinositol 3-Kinase
DNA Repair Enzymes
Motor Neurons
Transgenic Mice
Anterior Horn Cells
Oxidation-Reduction
Survival
Genes
Proteins
Amyotrophic Lateral Sclerosis
Immunoblotting
DNA Repair
Superoxide Dismutase
Spinal Cord
Immunohistochemistry

Keywords

  • Akt
  • ALS
  • Phosphatidylinositol 3-kinase
  • Redox factor
  • SOD1

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene. / Shiote, M.; Ilieva, H.; Nagano, I.; Murakami, T.; Hayashi, T.; Shoji, M.; Abe, K.

In: International Congress Series, Vol. 1252, No. C, 01.06.2003, p. 65-71.

Research output: Contribution to journalArticle

Shiote, M. ; Ilieva, H. ; Nagano, I. ; Murakami, T. ; Hayashi, T. ; Shoji, M. ; Abe, K. / Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene. In: International Congress Series. 2003 ; Vol. 1252, No. C. pp. 65-71.
@article{ad41152f815b49cbb66dc17e3052be8d,
title = "Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene",
abstract = "We examined expressions of phosphatidylinositol 3-kinase (PI3-K), Akt and redox factor-1 protein (Ref-1) in the spinal cord of transgenic mice with G93A mutant superoxide dismutase (SOD1) (Tg), a valuable model of human amyotrophic lateral sclerosis (ALS), at early and presymptomatic stage, 18 and 25 weeks of age. Significant decrease of PI3-K, and Akt in Tg/18 mice, and of PI3-K, Akt and Ref-1 in Tg/25 was observed on immunoblotting. Immunohistochemistry revealed the significant decrease of PI3-K, Akt and Ref-1 in spinal motor neurons of Tg/25 mice. No significant loss of anterior horn neurons was detected. Therefore, the decrease of survival signal or impairment of DNA repair in the spinal motor neurons precedes a subsequent death of anterior horn neurons, and may account for the mutant SOD1-mediated motor neuronal death in this model.",
keywords = "Akt, ALS, Phosphatidylinositol 3-kinase, Redox factor, SOD1",
author = "M. Shiote and H. Ilieva and I. Nagano and T. Murakami and T. Hayashi and M. Shoji and K. Abe",
year = "2003",
month = "6",
day = "1",
doi = "10.1016/S0531-5131(03)00069-4",
language = "English",
volume = "1252",
pages = "65--71",
journal = "International Congress Series",
issn = "0531-5131",
publisher = "Elsevier BV",
number = "C",

}

TY - JOUR

T1 - Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene

AU - Shiote, M.

AU - Ilieva, H.

AU - Nagano, I.

AU - Murakami, T.

AU - Hayashi, T.

AU - Shoji, M.

AU - Abe, K.

PY - 2003/6/1

Y1 - 2003/6/1

N2 - We examined expressions of phosphatidylinositol 3-kinase (PI3-K), Akt and redox factor-1 protein (Ref-1) in the spinal cord of transgenic mice with G93A mutant superoxide dismutase (SOD1) (Tg), a valuable model of human amyotrophic lateral sclerosis (ALS), at early and presymptomatic stage, 18 and 25 weeks of age. Significant decrease of PI3-K, and Akt in Tg/18 mice, and of PI3-K, Akt and Ref-1 in Tg/25 was observed on immunoblotting. Immunohistochemistry revealed the significant decrease of PI3-K, Akt and Ref-1 in spinal motor neurons of Tg/25 mice. No significant loss of anterior horn neurons was detected. Therefore, the decrease of survival signal or impairment of DNA repair in the spinal motor neurons precedes a subsequent death of anterior horn neurons, and may account for the mutant SOD1-mediated motor neuronal death in this model.

AB - We examined expressions of phosphatidylinositol 3-kinase (PI3-K), Akt and redox factor-1 protein (Ref-1) in the spinal cord of transgenic mice with G93A mutant superoxide dismutase (SOD1) (Tg), a valuable model of human amyotrophic lateral sclerosis (ALS), at early and presymptomatic stage, 18 and 25 weeks of age. Significant decrease of PI3-K, and Akt in Tg/18 mice, and of PI3-K, Akt and Ref-1 in Tg/25 was observed on immunoblotting. Immunohistochemistry revealed the significant decrease of PI3-K, Akt and Ref-1 in spinal motor neurons of Tg/25 mice. No significant loss of anterior horn neurons was detected. Therefore, the decrease of survival signal or impairment of DNA repair in the spinal motor neurons precedes a subsequent death of anterior horn neurons, and may account for the mutant SOD1-mediated motor neuronal death in this model.

KW - Akt

KW - ALS

KW - Phosphatidylinositol 3-kinase

KW - Redox factor

KW - SOD1

UR - http://www.scopus.com/inward/record.url?scp=85023074449&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85023074449&partnerID=8YFLogxK

U2 - 10.1016/S0531-5131(03)00069-4

DO - 10.1016/S0531-5131(03)00069-4

M3 - Article

VL - 1252

SP - 65

EP - 71

JO - International Congress Series

JF - International Congress Series

SN - 0531-5131

IS - C

ER -