Pericyte migration from the vascular wall in response to traumatic brain injury
Pericyte migration from the vascular wall in response to traumatic brain injury
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DOI：
10.1006/mvre.2000.2244
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发表时间：
2000-07-01
影响因子：
3.1
通讯作者：
Rafols, JA
中科院分区：
文献类型：
--
作者：
Dore-Duffy, P;Owen, C;Rafols, JA
任何对血脑屏障的扰动，无论是由于细胞生理学的变化还是由于直接损伤，都可能导致微血管功能障碍和疾病。我们在超微结构水平上检查了大鼠创伤性脑损伤模型中微血管周细胞的反应。在靠近撞击部位的区域，皮层周细胞在第一个小时内发生了一些变化。大约40%的周细胞从微血管位置迁移。迁移发生的同时，基底膜的腔面变薄，迁移细胞前表面尿激酶纤溶酶原激活剂受体的积累。迁移的周细胞似乎是有活力的，并在邻近的神经细胞中保持在血管周围的位置。同一切片的非迁移周细胞显示细胞质改变和核染色质改变，与快速退化过程一致。(C) 2000年学术出版社。
Any perturbation of the blood brain barrier, whether from changes in cell physiology or from direct injury, may result in microvascular dysfunction and disease. We examined, at the ultrastructural level, microvascular pericyte responses in a well-defined model of traumatic brain injury in the rat. In areas close to the site of impact cortical pericytes underwent a number of changes within the first hour. Approximately 40% of pericytes migrated from their microvascular location. Migration occurred concomitant with a thinning of the abluminal surface of the basal lamina and an accumulation of the receptor for the urokinase plasminogen activator on the leading surface of the migrating cell. Migrated pericytes appeared viable and remained in a perivascular location in the adjacent neuropil. Nonmigrating pericytes in the same section displayed cytoplasmic alterations and nuclear chromatin changes consistent with a rapid degenerative process. (C) 2000 Academic Press.