Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits

Masahiro Sakurai, Goro Takahashi, Koji Abe, Takashi Horinouchi, Yasuto Itoyama, Koichi Tabayashi

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Objective: The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. Because we previously reported that spinal motor neurons were probably lost as the result of programmed cell death, we investigated a possible mechanism of neuronal death by immunohistochemical analysis for Grp78 and caspase12. Methods: We used a rabbit spinal cord ischemia model with a balloon catheter. The spinal cord was removed at 8 hours or 1, 2, or 7 days after 15 minutes of transient ischemia. Histologic changes were studied with hematoxylin-eosin staining. Western blot analysis for Grp78 and caspase12, temporal profiles of Grp78 and caspase12 immunoreactivity, and double-label fluorescence immunocytochemical studies were performed. Results: The majority of motor neurons were preserved for 2 days but were selectively lost at 7 days of reperfusion. Western blot analysis revealed scarce immunoreactivity for Grp78 and caspase12 in the sham-operated spinal cords. However, immunoreactivity for Grp78 and caspase12 became apparent at 8 hours after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both Grp78 and caspase12 were positive at 8 hours of reperfusion in the same motor neurons that eventually die. Conclusion: This study demonstrated that immunoreactivities for both Grp78 and caspase12 were induced in the same motor neuron that eventually dies. These results suggest that endoplasmic reticulum stress was induced in motor neurons by transient spinal cord ischemia in rabbits.

Original languageEnglish
Pages (from-to)640-645
Number of pages6
JournalJournal of Thoracic and Cardiovascular Surgery
Volume130
Issue number3
DOIs
Publication statusPublished - Sep 2005

Fingerprint

Spinal Cord Ischemia
Endoplasmic Reticulum Stress
Motor Neurons
Rabbits
Ischemia
Reperfusion
Spinal Cord
Fluorescence
Western Blotting
Hematoxylin
Eosine Yellowish-(YS)
Spinal Cord Injuries
Cell Death
Catheters
Staining and Labeling

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits. / Sakurai, Masahiro; Takahashi, Goro; Abe, Koji; Horinouchi, Takashi; Itoyama, Yasuto; Tabayashi, Koichi.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 130, No. 3, 09.2005, p. 640-645.

Research output: Contribution to journalArticle

Sakurai, Masahiro ; Takahashi, Goro ; Abe, Koji ; Horinouchi, Takashi ; Itoyama, Yasuto ; Tabayashi, Koichi. / Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits. In: Journal of Thoracic and Cardiovascular Surgery. 2005 ; Vol. 130, No. 3. pp. 640-645.
@article{98b6d9237d294931bbd97a46b56fb8eb,
title = "Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits",
abstract = "Objective: The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. Because we previously reported that spinal motor neurons were probably lost as the result of programmed cell death, we investigated a possible mechanism of neuronal death by immunohistochemical analysis for Grp78 and caspase12. Methods: We used a rabbit spinal cord ischemia model with a balloon catheter. The spinal cord was removed at 8 hours or 1, 2, or 7 days after 15 minutes of transient ischemia. Histologic changes were studied with hematoxylin-eosin staining. Western blot analysis for Grp78 and caspase12, temporal profiles of Grp78 and caspase12 immunoreactivity, and double-label fluorescence immunocytochemical studies were performed. Results: The majority of motor neurons were preserved for 2 days but were selectively lost at 7 days of reperfusion. Western blot analysis revealed scarce immunoreactivity for Grp78 and caspase12 in the sham-operated spinal cords. However, immunoreactivity for Grp78 and caspase12 became apparent at 8 hours after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both Grp78 and caspase12 were positive at 8 hours of reperfusion in the same motor neurons that eventually die. Conclusion: This study demonstrated that immunoreactivities for both Grp78 and caspase12 were induced in the same motor neuron that eventually dies. These results suggest that endoplasmic reticulum stress was induced in motor neurons by transient spinal cord ischemia in rabbits.",
author = "Masahiro Sakurai and Goro Takahashi and Koji Abe and Takashi Horinouchi and Yasuto Itoyama and Koichi Tabayashi",
year = "2005",
month = "9",
doi = "10.1016/j.jtcvs.2005.01.007",
language = "English",
volume = "130",
pages = "640--645",
journal = "Journal of Thoracic and Cardiovascular Surgery",
issn = "0022-5223",
publisher = "Mosby Inc.",
number = "3",

}

TY - JOUR

T1 - Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits

AU - Sakurai, Masahiro

AU - Takahashi, Goro

AU - Abe, Koji

AU - Horinouchi, Takashi

AU - Itoyama, Yasuto

AU - Tabayashi, Koichi

PY - 2005/9

Y1 - 2005/9

N2 - Objective: The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. Because we previously reported that spinal motor neurons were probably lost as the result of programmed cell death, we investigated a possible mechanism of neuronal death by immunohistochemical analysis for Grp78 and caspase12. Methods: We used a rabbit spinal cord ischemia model with a balloon catheter. The spinal cord was removed at 8 hours or 1, 2, or 7 days after 15 minutes of transient ischemia. Histologic changes were studied with hematoxylin-eosin staining. Western blot analysis for Grp78 and caspase12, temporal profiles of Grp78 and caspase12 immunoreactivity, and double-label fluorescence immunocytochemical studies were performed. Results: The majority of motor neurons were preserved for 2 days but were selectively lost at 7 days of reperfusion. Western blot analysis revealed scarce immunoreactivity for Grp78 and caspase12 in the sham-operated spinal cords. However, immunoreactivity for Grp78 and caspase12 became apparent at 8 hours after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both Grp78 and caspase12 were positive at 8 hours of reperfusion in the same motor neurons that eventually die. Conclusion: This study demonstrated that immunoreactivities for both Grp78 and caspase12 were induced in the same motor neuron that eventually dies. These results suggest that endoplasmic reticulum stress was induced in motor neurons by transient spinal cord ischemia in rabbits.

AB - Objective: The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. Because we previously reported that spinal motor neurons were probably lost as the result of programmed cell death, we investigated a possible mechanism of neuronal death by immunohistochemical analysis for Grp78 and caspase12. Methods: We used a rabbit spinal cord ischemia model with a balloon catheter. The spinal cord was removed at 8 hours or 1, 2, or 7 days after 15 minutes of transient ischemia. Histologic changes were studied with hematoxylin-eosin staining. Western blot analysis for Grp78 and caspase12, temporal profiles of Grp78 and caspase12 immunoreactivity, and double-label fluorescence immunocytochemical studies were performed. Results: The majority of motor neurons were preserved for 2 days but were selectively lost at 7 days of reperfusion. Western blot analysis revealed scarce immunoreactivity for Grp78 and caspase12 in the sham-operated spinal cords. However, immunoreactivity for Grp78 and caspase12 became apparent at 8 hours after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both Grp78 and caspase12 were positive at 8 hours of reperfusion in the same motor neurons that eventually die. Conclusion: This study demonstrated that immunoreactivities for both Grp78 and caspase12 were induced in the same motor neuron that eventually dies. These results suggest that endoplasmic reticulum stress was induced in motor neurons by transient spinal cord ischemia in rabbits.

UR - http://www.scopus.com/inward/record.url?scp=24644482017&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=24644482017&partnerID=8YFLogxK

U2 - 10.1016/j.jtcvs.2005.01.007

DO - 10.1016/j.jtcvs.2005.01.007

M3 - Article

C2 - 16153907

AN - SCOPUS:24644482017

VL - 130

SP - 640

EP - 645

JO - Journal of Thoracic and Cardiovascular Surgery

JF - Journal of Thoracic and Cardiovascular Surgery

SN - 0022-5223

IS - 3

ER -