Induction of phosphatidylinositol 3-kinase and serine-threonine kinase-like immunoreactivity in rabbit spinal cord after transient ischemia

Masahiro Sakurai, Takeshi Hayashi, Koji Abe, Yasuto Itoyuama, Koichi Tabayashi

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model of rabbit spinal cord ischemia. Using this model, the inductions of phosphatidylinositol 3-kinase (PI3-k) and serine-threonine kinase (Akt) were investigated with immunohistochemical analyses for up to 7 days of the reperfusion following 15 min of ischemia in rabbit spinal cord. It has been demonstrated that both PI3-k and its downstream effector, Akt mediate growth factor-induced neuronal survival. Spinal cord sections from animals sacrificed at 8 h, 1, 2, and 7 days following the 15 min of ischemia were immunohistochemically evaluated using monoclonal antibodies for PI3-k and Akt. Following the 15 min of ischemia, the majority of the motor neurons showed selective cell death at 7 days of reperfusion. Immunoreactivity of PI3-k and Akt were induced at 8 h of reperfusion selectively in motor neuron cells. No glial cells and inter neurons were stained in the spinal cord sections. The activation of PI3-k and Akt protein at the early stage of reperfusion may be one of the factors responsible for the delay in neuronal death after spinal cord ischemia.

Original languageEnglish
Pages (from-to)17-20
Number of pages4
JournalNeuroscience Letters
Volume302
Issue number1
DOIs
Publication statusPublished - Apr 13 2001

Fingerprint

Phosphatidylinositol 3-Kinase
Protein-Serine-Threonine Kinases
Motor Neurons
Spinal Cord
Ischemia
Reperfusion
Rabbits
Spinal Cord Ischemia
Spinal Cord Injuries
Neuroglia
Intercellular Signaling Peptides and Proteins
Cell Death
Monoclonal Antibodies
Neurons
Proteins

Keywords

  • Phosphatidylinositol 3-kinase
  • Serine-threonine kinase
  • Spinal cord ischemia

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Induction of phosphatidylinositol 3-kinase and serine-threonine kinase-like immunoreactivity in rabbit spinal cord after transient ischemia. / Sakurai, Masahiro; Hayashi, Takeshi; Abe, Koji; Itoyuama, Yasuto; Tabayashi, Koichi.

In: Neuroscience Letters, Vol. 302, No. 1, 13.04.2001, p. 17-20.

Research output: Contribution to journalArticle

Sakurai, Masahiro ; Hayashi, Takeshi ; Abe, Koji ; Itoyuama, Yasuto ; Tabayashi, Koichi. / Induction of phosphatidylinositol 3-kinase and serine-threonine kinase-like immunoreactivity in rabbit spinal cord after transient ischemia. In: Neuroscience Letters. 2001 ; Vol. 302, No. 1. pp. 17-20.
@article{62620963a27d458f92d156d8a7e0f970,
title = "Induction of phosphatidylinositol 3-kinase and serine-threonine kinase-like immunoreactivity in rabbit spinal cord after transient ischemia",
abstract = "The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model of rabbit spinal cord ischemia. Using this model, the inductions of phosphatidylinositol 3-kinase (PI3-k) and serine-threonine kinase (Akt) were investigated with immunohistochemical analyses for up to 7 days of the reperfusion following 15 min of ischemia in rabbit spinal cord. It has been demonstrated that both PI3-k and its downstream effector, Akt mediate growth factor-induced neuronal survival. Spinal cord sections from animals sacrificed at 8 h, 1, 2, and 7 days following the 15 min of ischemia were immunohistochemically evaluated using monoclonal antibodies for PI3-k and Akt. Following the 15 min of ischemia, the majority of the motor neurons showed selective cell death at 7 days of reperfusion. Immunoreactivity of PI3-k and Akt were induced at 8 h of reperfusion selectively in motor neuron cells. No glial cells and inter neurons were stained in the spinal cord sections. The activation of PI3-k and Akt protein at the early stage of reperfusion may be one of the factors responsible for the delay in neuronal death after spinal cord ischemia.",
keywords = "Phosphatidylinositol 3-kinase, Serine-threonine kinase, Spinal cord ischemia",
author = "Masahiro Sakurai and Takeshi Hayashi and Koji Abe and Yasuto Itoyuama and Koichi Tabayashi",
year = "2001",
month = "4",
day = "13",
doi = "10.1016/S0304-3940(01)01609-3",
language = "English",
volume = "302",
pages = "17--20",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Induction of phosphatidylinositol 3-kinase and serine-threonine kinase-like immunoreactivity in rabbit spinal cord after transient ischemia

AU - Sakurai, Masahiro

AU - Hayashi, Takeshi

AU - Abe, Koji

AU - Itoyuama, Yasuto

AU - Tabayashi, Koichi

PY - 2001/4/13

Y1 - 2001/4/13

N2 - The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model of rabbit spinal cord ischemia. Using this model, the inductions of phosphatidylinositol 3-kinase (PI3-k) and serine-threonine kinase (Akt) were investigated with immunohistochemical analyses for up to 7 days of the reperfusion following 15 min of ischemia in rabbit spinal cord. It has been demonstrated that both PI3-k and its downstream effector, Akt mediate growth factor-induced neuronal survival. Spinal cord sections from animals sacrificed at 8 h, 1, 2, and 7 days following the 15 min of ischemia were immunohistochemically evaluated using monoclonal antibodies for PI3-k and Akt. Following the 15 min of ischemia, the majority of the motor neurons showed selective cell death at 7 days of reperfusion. Immunoreactivity of PI3-k and Akt were induced at 8 h of reperfusion selectively in motor neuron cells. No glial cells and inter neurons were stained in the spinal cord sections. The activation of PI3-k and Akt protein at the early stage of reperfusion may be one of the factors responsible for the delay in neuronal death after spinal cord ischemia.

AB - The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model of rabbit spinal cord ischemia. Using this model, the inductions of phosphatidylinositol 3-kinase (PI3-k) and serine-threonine kinase (Akt) were investigated with immunohistochemical analyses for up to 7 days of the reperfusion following 15 min of ischemia in rabbit spinal cord. It has been demonstrated that both PI3-k and its downstream effector, Akt mediate growth factor-induced neuronal survival. Spinal cord sections from animals sacrificed at 8 h, 1, 2, and 7 days following the 15 min of ischemia were immunohistochemically evaluated using monoclonal antibodies for PI3-k and Akt. Following the 15 min of ischemia, the majority of the motor neurons showed selective cell death at 7 days of reperfusion. Immunoreactivity of PI3-k and Akt were induced at 8 h of reperfusion selectively in motor neuron cells. No glial cells and inter neurons were stained in the spinal cord sections. The activation of PI3-k and Akt protein at the early stage of reperfusion may be one of the factors responsible for the delay in neuronal death after spinal cord ischemia.

KW - Phosphatidylinositol 3-kinase

KW - Serine-threonine kinase

KW - Spinal cord ischemia

UR - http://www.scopus.com/inward/record.url?scp=0035853570&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035853570&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(01)01609-3

DO - 10.1016/S0304-3940(01)01609-3

M3 - Article

VL - 302

SP - 17

EP - 20

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1

ER -