SCAR FORMATION AFTER DRUG-INDUCED COCHLEAR INSULT
SCAR FORMATION AFTER DRUG-INDUCED COCHLEAR INSULT
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DOI：
10.1016/0378-5955(91)90034-7
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发表时间：
1991-02-01
期刊：
影响因子：
2.8
通讯作者：
ALTSCHULER, RA
中科院分区：
文献类型：
--
作者：
RAPHAEL, Y;ALTSCHULER, RA
利用组织化学和电子显微镜研究了药物诱导的毛细胞变性过程中豚鼠柯蒂氏器官的结构和分子变化。 肌动蛋白丝从角质板和静纤毛消失。 垂死毛细胞的顶端区域出现富含肌动蛋白的桥。 两个支持细胞形成给定毛细胞的疤痕。 支持细胞扩张并侵入 Nuel 空间，然后侵入先前被毛细胞占据的区域。 疤痕区域被细胞角蛋白标记。 在这项研究中，毛细胞的顶端域是细胞退化的最后部分。 毛细胞变性在时间上与疤痕形成同时发生。 我们将由此产生的疤痕定义为“I 型”疤痕。 结果提供了有关 I 型疤痕分子组成的初步信息，并提出了疤痕形成动力学的结构基础。
Structural and molecular changes in the guinea pig organ of Corti were studied using histochemistry and electron microscopy in the course of drug-induced hair cell degeneration. Actin filaments disappear from the cuticular plate and the stereocilia. An actin-rich bridge appears in the apical region of dying hair cells. Two supporting cells form a scar for a given hair cell. The supporting cells expand and invade the spaces of Nuel and then the region previously occupied by the hair cell. The scar region becomes cytokeratin-labeled. In this study, the apical domain of the hair cell is the last part of the cell to degenerate. Hair cell degeneration coincides temporally with scar formation. We define the resulting scar as a 'type I' scar. The results provide preliminary information about the molecular composition of the type I scar and suggest a structural basis for the dynamics of scar formation.