Stem cell factor prevents neuronal cell apoptosis after acute spinal cord injury.
METHODS
A rat spinal cord injury (SCI) model and immunohistochemistry were used to examine the levels of expression of stem cell factor and c-kit. In addition, we examined whether intraperitoneal administration of stem cell factor could prevent neural cells apoptosis after acute SCI.


OBJECTIVE
To evaluate the antiapoptotic effect of stem cell factor after SCI.


BACKGROUND
It is well known that the mode of delayed neuronal and glial cell death after SCI is apoptosis. Inhibition of apoptosis might thus promote neurologic improvement after SCI. Stem cell factor and its receptor c-kit exhibit pleiotropic effects in early hematopoiesis, and are also known to prevent hematopoietic progenitor cell apoptosis. Stem cell factor has recently been reported to be a survival factor for neural stem cells in vitro. We examined the levels of expression of stem cell factor and c-kit in normal and injured rat spinal cord. In addition, we examined whether stem cell factor prevents neural cell apoptosis after acute SCI.


METHODS
We examined the expression of stem cell factor and c-kit in spinal cord after injury by quantitative RT-PCR and immunohistochemistry. Antiapoptotic effects of stem cell factor were examined using rats with SCI that received stem cell factor intraperitoneally, and were examined immunohistochemically with anticleaved PARP antibody and antiactive caspase-3 antibody between 1 and 3 days after injury.


RESULTS
Upregulation of stem cell factor and c-kit expression occured after SCI. We also found that neurons express stem cell factor, and neurons and oligodendrocytes express c-kit after SCI. In addition, intraperitoneal administration of stem cell factor prevented spinal neural cells apoptosis after injury.


CONCLUSIONS
These findings suggest the possibility that stem cell factor, a hematopoietic cytokine, could be useful as an agent for treatment of SCI.
Yamasaki
Kouhei
K
Department of Orthopaedic Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Setoguchi
Takao
T
Takenouchi
Takeshi
T
Yone
Kazunori
K
Komiya
Setsuro
S
D000208:Acute Disease; D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007274:Injections, Intraperitoneal; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000378:metabolism*; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D019089:Stem Cell Factor / Q000008:administration & dosage / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation
D018696:Neuroprotective Agents; D012333:RNA, Messenger; D019089:Stem Cell Factor; D019009:Proto-Oncogene Proteins c-kit