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on February 16, 2006

Stroke. 2006
Published online before print February 16, 2006, doi: 10.1161/01.STR.0000206280.30972.21
A more recent version of this article appeared on April 1, 2006
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Submitted on August 21, 2005
Revised on November 10, 2005
Accepted on December 7, 2005

Neuroprotective Effects of Activated Protein C Through Induction of Insulin-Like Growth Factor-1 (IGF-1), IGF-1 Receptor, and Its Downstream Signal Phosphorylated Serine-Threonine Kinase After Spinal Cord Ischemia in Rabbits

Takashi Yamauchi MD; Masahiro Sakurai MD, PhD; Koji Abe MD, PhD; Hiroshi Takano MD, PhD; and Yoshiki Sawa MD, PhD*

From the Department of Cardiovascular Surgery (T.Y., H.T., Y.S.), Osaka University Graduate School of Medicine, Japan; Department of Cardiovascular Surgery (M.S.), National Hospital Organization Sendai Medical Center, Sendai Japan; and Department of Neurology (K.A.), Okayama University Graduate School of Medicine, Japan.

* To whom correspondence should be addressed. E-mail: sawa{at}surg1.med.osaka-u.ac.jp.

Background and Purpose--Activated protein C (APC) has beneficial effects on ischemia reperfusion injury in neuron. However, the possible mechanism of such beneficial effects is not fully understood. The aim of this study was to investigate the effects and possible mechanisms of APC on ischemic spinal cord damage.

Methods--After induction of spinal cord ischemia, APC (group A) or vehicle (group I) was injected intravenously. Severity of ischemic damage was analyzed by counting the number of motor neurons. To investigate the mechanisms by which APC prevents ischemic spinal cord damage, we performed immunoreactivity and Western blotting of insulin-like growth factor 1 (IGF-1), IGF-1 receptor, and phosphorylated serine-threonine kinase (p-Akt).

Results--APC eased the functional deficits and increased the number of motor neurons after ischemia. Immunoreactivity of IGF-1 in group A was stronger than in group I at 8 hours after reperfusion but was at the same level at 1 day. Induction of IGF-1 receptor and the downstream factor p-Akt was stronger and more prolonged in group A.

Conclusions--These results indicate that induction of IGF-1, IGF-1 receptor, and p-Akt might partially explain the neuroprotective effects of APC after transient spinal cord ischemia in rabbit.
Key words: spinal cord • ischemia • paraplegia • insulin-like growth factor I • protein C




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L. O. Mosnier, B. V. Zlokovic, and J. H. Griffin
The cytoprotective protein C pathway
Blood, April 15, 2007; 109(8): 3161 - 3172.
[Abstract] [Full Text] [PDF]


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