Identification of autotaxin as a neurite retraction-inducing factor of PC12 cells in cerebrospinal fluid and its possible sources
Identification of autotaxin as a neurite retraction-inducing factor of PC12 cells in cerebrospinal fluid and its possible sources
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DOI：
10.1111/j.1471-4159.2004.02933.x
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发表时间：
2005-02-01
影响因子：
4.7
通讯作者：
Okajima, F
中科院分区：
文献类型：
--
作者：
Sato, K;Malchinkhuu, E;Okajima, F
脑脊液（CSF）诱导分化的PC 12细胞的神经突收缩;在15分钟内观察到的行动（快速反应）和活动进一步增加，直到6小时（长效反应）在暴露的CSF的细胞。CSF的行动是敏感的单甘油酯脂肪酶和减少同源脱敏与溶血磷脂酸（LPA）和预处理与LPA受体拮抗剂Ki 16425。虽然新鲜脑脊液中含有一定量的LPA，但在培养过程中，培养液中的LPA含量增加。外源性LPA模仿的快速反应，和一个长效的反应是由重组自分泌运动因子，溶血磷脂酶D（溶血PLD）复制。虽然在CSF中未检测到溶血PLD底物溶血磷脂酰胆碱（LPC），但在CSF中检测到溶血PLD活性和类似于120-kDa自分泌运动因子的蛋白。另一方面，LPC，但不是溶血PLD活性中检测到的条件培养基中的PC 12细胞培养物没有CSF。在检查的神经细胞中，软脑膜细胞表达最高的lyso-PLD活性和autotaxin蛋白。这些结果表明，软脑膜细胞可能是自分泌运动因子的来源之一，自分泌运动因子可能在LPA的产生中起关键作用，从而调节轴突和神经突的形态变化。
Cerebrospinal fluid (CSF) induced neurite retraction of differentiated PC12 cells; the action was observed in 15 min (a rapid response) and the activity further increased until 6 h (a long-acting response) during exposure of CSF to the cells. The CSF action was sensitive to monoglyceride lipase and diminished by homologous desensitization with lysophosphatidic acid (LPA) and by pretreatment with an LPA receptor antagonist Ki16425. Although fresh CSF contains LPA to some extent, the LPA content in the medium was increased during culture of PC12 cells with CSF. The rapid response was mimicked by exogenous LPA, and a long-acting response was duplicated by a recombinant autotaxin, lysophospholipase D (lyso-PLD). Although the lyso-PLD substrate lysophosphatidylcholine (LPC) was not detected in CSF, lyso-PLD activity and an similar to120-kDa autotaxin protein were detected in CSF. On the other hand, LPC but not lyso-PLD activity was detected in the conditioned medium of a PC12 cell culture without CSF. Among neural cells examined, leptomeningeal cells expressed the highest lyso-PLD activity and autotaxin protein. These results suggest that leptomeningeal cells may work as one of the sources for autotaxin, which may play a critical role in LPA production and thereby regulate axonal and neurite morphological change.