LPA-mediated demyelination in ex vivo culture of dorsal root
LPA-mediated demyelination in ex vivo culture of dorsal root
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DOI：
10.1016/j.neuint.2006.09.003
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发表时间：
2007-01-01
影响因子：
4.2
通讯作者：
Ueda, Hiroshi
中科院分区：
文献类型：
--
作者：
Fujita, Ryousuke;Kiguchi, Norikazu;Ueda, Hiroshi
溶血磷脂酸（LPA）引起神经性疼痛，伴有感觉纤维脱髓鞘。在背根（DR）离体培养中，在扫描和透射电镜分析中，0.1 μ M LPA的加入在24小时引起特征性脱髓鞘。此外，由于Remak束中Schwarm细胞的分隔损失，观察到C纤维之间的直接接触。LPA诱导的DR的脱环在0.01和IM之间的范围内是浓度依赖性的，并且分别被BoNT/C3和Y-27632（RhoA和Rho激酶抑制剂）消除。有无背根神经节的标本脱髓鞘程度相当。LPA还引起髓磷脂蛋白如髓磷脂碱性蛋白（MBP）和髓磷脂蛋白零（MPZ）的下调至对照的约70%。所有这些发现表明，在神经损伤引起的神经病理性疼痛中观察到的脱髓鞘通过LPA对雪旺细胞的直接作用而发生。(c)2006爱思唯尔有限公司保留所有权利。
Lysophosphatidic acid (LPA) causes neuropathic pain with demyelination in sensory fibers. In dorsal root (DR) ex vivo culture, the addition of 0.1 mu M LPA caused a characteristic demyelination at 24 h in scanning and transmission electron microscopy analyses. Moreover, direct contact between C-fibers due to loss of partition by Schwarm cell in Remak bundles was observed. LPA-induced demyclination of DR was concentration-dependent in the range between 0.01 and I M, and was abolished by BoNT/C3 and Y-27632, a RhoA and Rho kinase inhibitor, respectively. The demyelination was equivalent between the preparations with and without dorsal root ganglion. LPA also caused a down-regulation of myelin proteins, such as myelin basic protein (MBP) and myelin protein zero (MPZ) to approximately 70% of control. All these findings suggest that the demyelination observed in the neuropathic pain due to nerve injury occurs through a direct action of LPA on Schwann cells. (c) 2006 Elsevier Ltd. All rights reserved.