Yamasaki Kouhei, Setoguchi Takao, Takenouchi Takeshi, Yone Kazunori, Komiya Setsuro
Department of Orthopaedic Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Spine (Phila Pa 1976). 2009 Feb 15;34(4):323-7. doi: 10.1097/BRS.0b013e318193a1de.
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.
To evaluate the antiapoptotic effect of stem cell factor after SCI.
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.
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.
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.
These findings suggest the possibility that stem cell factor, a hematopoietic cytokine, could be useful as an agent for treatment of SCI.
采用大鼠脊髓损伤（SCI）模型和免疫组织化学方法检测干细胞因子和c-kit的表达水平。此外，我们还研究了腹腔注射干细胞因子是否能预防急性脊髓损伤后神经细胞凋亡。
评估脊髓损伤后干细胞因子的抗凋亡作用。
众所周知，脊髓损伤后神经元和神经胶质细胞延迟性死亡的方式是凋亡。因此，抑制凋亡可能会促进脊髓损伤后的神经功能改善。干细胞因子及其受体c-kit在早期造血过程中具有多效性作用，并且已知能预防造血祖细胞凋亡。最近有报道称干细胞因子在体外是神经干细胞的存活因子。我们检测了正常和损伤大鼠脊髓中干细胞因子和c-kit的表达水平。此外，我们还研究了干细胞因子是否能预防急性脊髓损伤后神经细胞凋亡。
通过定量逆转录聚合酶链反应（RT-PCR）和免疫组织化学检测损伤后脊髓中干细胞因子和c-kit的表达。使用腹腔注射干细胞因子的脊髓损伤大鼠研究干细胞因子的抗凋亡作用，并在损伤后1至3天用抗裂解聚（ADP-核糖）聚合酶（PARP）抗体和抗活性半胱天冬酶-3抗体进行免疫组织化学检测。
脊髓损伤后干细胞因子和c-kit表达上调。我们还发现神经元表达干细胞因子，脊髓损伤后神经元和少突胶质细胞表达c-kit。此外，腹腔注射干细胞因子可预防损伤后脊髓神经细胞凋亡。
这些发现提示造血细胞因子干细胞因子有可能作为一种治疗脊髓损伤的药物。
