Ependymal denudation and alterations of the subventricular zone occur in human fetuses with a moderate communicating hydrocephalus
Ependymal denudation and alterations of the subventricular zone occur in human fetuses with a moderate communicating hydrocephalus
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DOI：
10.1097/01.jnen.0000171648.86718.bb
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发表时间：
2005-07-01
影响因子：
3.2
通讯作者：
Rodríguez, EM
中科院分区：
文献类型：
--
作者：
Domínguez-Pinos, MD;Páez, P;Rodríguez, EM
在突变型啮齿动物中，室管膜脱落发生在胎儿期早期，先于交流性脑积水的发病，是该病病因学中的一个关键事件。本研究旨在获得16- 40周大的人源性脑积水胎儿（n = 8）与同龄无神经病理改变的胎儿（n = 15）相比是否发生室管膜剥落的证据。通过脑导水管和侧脑室壁的切片进行凝集素结合和免疫细胞化学处理，使用针对室管膜、星形胶质细胞、神经母细胞和巨噬细胞标记物的抗体。用抗腔室素作为胎儿室管膜的功能标志物。在人胎儿室管膜分化过程中，结构和功能分子标记存在差异表达。导水管室管膜和侧脑室的剥落发生在所有发生交通性脑积水的胎儿中，包括所研究的最年轻的胎儿。剥落面积随胎龄的增加而增加。这种可能性是先进的，在许多或大多数情况下，人类胎儿脑积水有一个共同的缺陷，在室管膜细胞谱系导致室管膜脱离。有证据表明，在患有脑积水的人类胎儿中，在胎儿生命期间发生了修复剥落区域的过程。在脑积水胎儿中，侧脑室室管膜脱离导致(1)生发室管膜区缺失，(2)室下区紊乱，(3)神经母细胞异常迁移至脑室腔。因此，脑积水胎儿的室管膜层脱离不仅与脑积水的发病机制有关，而且与异常的神经发生有关。
In mutant rodents, ependymal denudation occurs early in fetal life, preceding the onset of a communicating hydrocephalus, and is a key event in the etiology of this disease. The present investigation was designed to obtain evidence whether or not ependymal denudation occurs in 16- to 40-week-old human fetuses developing a communicating hydrocephalus (n = 8) as compared to fetuses of similar ages with no neuropathologic alterations (n = 15). Sections through the walls of the cerebral aqueduct and lateral ventricles were processed for lectin binding and immunocytochemistry using antibodies against ependyma, astroglia, neuroblasts, and macrophages markers. Anti-caveolin was used as a functional marker of the fetal ependyma. The structural and functional molecular markers are differentially expressed throughout the differentiation of the human fetal ependyma. Denudation of the ependyma of the aqueduct and lateral ventricles occurred in all fetuses developing a communicating hydrocephalus, including the youngest ones studied. The denuded surface area increased in parallel with the fetus age. The possibility is advanced that in many or most cases of human fetal hydrocephalus there is a common defect at the ependymal cell lineage leading to ependymal detachment. Evidence was obtained that in hydrocephalic human fetuses a process to repair the denuded areas takes place during the fetal life. In hydrocephalic fetuses, detachment of the ependyma of the lateral ventricles resulted in the (i) loss of the germinal ependymal zone, (ii) disorganization of the subventricular zone and, (iii) abnormal migration of neuroblasts into the ventricular cavity. Thus, detachment of the ependymal layer in hydrocephalic fetuses would not only be associated with the pathogenesis of hydrocephalus but also to abnormal neurogenesis.