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首页> 外文期刊>Journal of Neuroscience Research >Bone marrow mononuclear cells migrate to the demyelinated sciatic nerve and transdifferentiate into Schwann cells after nerve injury: attempt at a peripheral nervous system intrinsic repair mechanism.
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Bone marrow mononuclear cells migrate to the demyelinated sciatic nerve and transdifferentiate into Schwann cells after nerve injury: attempt at a peripheral nervous system intrinsic repair mechanism.

机译：神经损伤后，骨髓单个核细胞迁移至脱髓鞘的坐骨神经，并转分化为雪旺细胞：尝试建立周围神经系统的内在修复机制。

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In the present work, we analyzed whether endogenous and/or transplanted bone marrow mononuclear cells (BMMC) migrate spontaneously to the crushed sciatic nerve and whether they transdifferentiate into Schwann cells (SC) in order to help repair the damaged tissue. We also studied both the immunohistochemical evolution of myelin proteins MBP and P(0) and the myelin composition of both the proximal and distal stumps of the crushed sciatic nerve to determine the demyelination-remyelination period. Immunohistochemical analysis of crushed animals showed that the degeneration process consists of loss of nerve fiber integrity accompanied by degradation of myelin basic proteins MBP and P(0) , which is anticipated by protein cluster formation. The remyelination process appears as a recovery in nerve fiber structure as well as in MBP and P(0) immunoreactivity; results obtained studying isolated myelin from the crushed sciatic nerve show a strong correlation between them. As opposed to demyelination, axonal damage is observed for a short period of time and takes place mostly in the crush area and the segments adjacent to the lesion. Evidence of spontaneous migration of endogenous or intravascularly transplanted BMMC (CD34(+) and vimentin(+) ) is found during the demyelination period exclusively to the injured sciatic nerve. Once migration takes place, transdifferentiation to SC is observed. Such migration and transdifferentiation processes might be inferred to constitute a spontaneous repair mechanism after nerve injury.
机译：在目前的工作中，我们分析了内源性和/或移植的骨髓单核细胞（BMMC）是否自发地迁移至破碎的坐骨神经，以及它们是否转分化为雪旺细胞（SC）以帮助修复受损的组织。我们还研究了髓磷脂蛋白MBP和P（0）的免疫组织化学演变，以及坐骨神经近端和远端残端的髓鞘组成，以确定脱髓鞘-再髓鞘形成时期。压迫动物的免疫组织化学分析表明，变性过程包括神经纤维完整性的丧失以及髓磷脂碱性蛋白MBP和P（0）的降解，这可以通过蛋白簇的形成来预期。髓鞘再生过程表现为神经纤维结构以及MBP和P（0）免疫反应性的恢复;研究从坐骨神经压迫中分离出的髓鞘蛋白得到的结果表明它们之间有很强的相关性。与脱髓鞘相反，在短时间内观察到了轴突损伤，它主要发生在挤压区和病变附近的部分。内源性或血管内移植的BMMC（CD34（+）和波形蛋白（+））自发迁移的证据是在脱髓鞘期间仅转移至受损的坐骨神经。一旦发生迁移，观察到向SC的转分化。可以推断这种迁移和转分化过程构成了神经损伤后的自发修复机制。

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