Spontaneous recovery of cochlear fibrocytes after severe degeneration caused by acute energy failure.
Spontaneous recovery of cochlear fibrocytes after severe degeneration caused by acute energy failure.
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DOI：
10.3389/fphar.2014.00198
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发表时间：
2014
影响因子：
5.6
通讯作者：
Mizutari K
中科院分区：
文献类型：
--
作者：
Mizutari K
耳蜗外侧壁区域的耳蜗纤维细胞在内耳离子和流体稳态的调节中起关键作用，尽管这些是非感觉细胞。沿着其他非感觉细胞，螺旋韧带中的纤维细胞在损伤后可以自我再生。然而，由于没有合适的纤维细胞特异性变性模型，耳蜗纤维细胞再生的研究一直很困难。因此，我们分析了耳蜗纤维细胞使用大鼠模型的急性耳蜗能量衰竭引起的线粒体毒素。该模型是独特的，因为听力损失是由耳蜗外侧壁中的纤维细胞凋亡而不是由感觉细胞损伤引起的。尽管该模型涉及耳蜗外侧壁的严重损伤，但在没有任何治疗的情况下发生延迟的自发再生。此外，部分听力恢复伴随着耳蜗外侧壁的形态重塑。关于耳蜗纤维细胞的自发恢复，有两种假设是可以想象的。一种是残留的耳蜗纤维细胞自发增殖，随后是外侧壁功能区的重塑。另一个原因是某些外源性细胞如骨髓源性细胞促进了外侧壁的形态和功能恢复。通过这些机制促进外侧壁的恢复可能是一种新的治疗策略。
Cochlear fibrocytes in the lateral wall region play a critical role in the regulation of inner ear ion and fluid homeostasis, although these are non-sensory cells. Along with other non-sensory cells, fibrocytes in the spiral ligament have been reported to repopulate themselves after damage. However, the studies of regeneration of cochlear fibrocytes have been difficult because a suitable fibrocyte-specific degeneration model did not exist. Therefore, we analyzed cochlear fibrocytes using a rat model of acute cochlear energy failure induced by a mitochondrial toxin. This model is unique because hearing loss is caused by apoptosis of fibrocytes in the cochlear lateral wall not by damage to sensory cells. Although this model involves severe damage to the cochlear lateral wall, delayed spontaneous regeneration occurs without any treatment. Moreover, partial hearing recovery is accompanied by morphological remodeling of the cochlear lateral wall. Two hypotheses are conceivable regarding this spontaneous recovery of cochlear fibrocytes. One is that residual cochlear fibrocytes proliferate spontaneously, followed by remodeling of the functional region of the lateral wall. Another is that some foreign cells such as bone marrow-derived cells promote morphological and functional recovery of the lateral wall. Acceleration of the lateral wall recovery promoted by these mechanisms may be a new therapeutic strategy against hearing loss.
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影响因子：
2.8
作者：
Shi X
通讯作者：
Shi X
影响因子：
6
作者：
Kamiya, Kazusaku;Fujinami, Yoshiaki;Matsunaga, Tatsuo
通讯作者：
Matsunaga, Tatsuo
影响因子：
2.8
作者：
Labbé, D;Teranishi, M;Michel, O
通讯作者：
Michel, O
影响因子：
3.2
作者：
Crouch, JJ;Sakaguchi, N;Schulte, BA
通讯作者：
Schulte, BA
DOI：
10.1007/bf00186783
发表时间：
1995-02-01
期刊：
ANATOMY AND EMBRYOLOGY
影响因子：
--
作者：
KIKUCHI, T;KIMURA, RS;ADAMS, JC
通讯作者：
ADAMS, JC