Selective activation of nuclear factor kappa B in the cochlea by sensory and inflammatory stress.
Selective activation of nuclear factor kappa B in the cochlea by sensory and inflammatory stress.
复制标题
DOI：
10.1016/j.neuroscience.2009.02.073
复制
发表时间：
2009-05-05
期刊：
影响因子：
3.3
通讯作者：
中科院分区：
文献类型：
--
作者：
由机械应力触发的损伤反应途径可能会在整个进化过程中得到保留。然而，使用 NF-κB 报告小鼠，我们在此表明，这种系统发育上较新的转录因子在哺乳动物内耳对机械感觉应激的反应中发挥着重要作用。 NF-κB 的保护作用既不在感觉上皮细胞中发挥作用，也不在非感觉上皮细胞中发挥作用，而是在螺旋韧带和螺旋缘内的结缔组织细胞中发挥作用。在螺旋韧带中，主要是 I 型纤维细胞在噪声暴露后被激活，而 II 型纤维细胞在全身炎症应激后被激活。人类免疫介导和声损伤介导的听力损失综合征可能部分归因于 II 型和 I 型纤维细胞分别对全身炎症应激和声损伤的脆弱性。在这项体内研究中，在内耳中发现了意想不到的细胞特异性和应激特异性 NF-κB 激活，这表明这种方法可能在证明包括大脑在内的其他组织中应激反应的类似专业化方面具有广泛的应用。
Damage response pathways triggered by mechanical stress might reasonably be expected to be conserved throughout evolution. However, using an NF-κB reporter mouse we show here that this phylogenetically recent transcription factor plays a major role in the response to mechanosensory stress in the mammalian inner ear. The protective action of NF-κB is exerted in neither sensory nor non-sensory epithelial cells, but rather in connective tissue cells within the spiral ligament and spiral limbus. In the spiral ligament, predominantly type I fibrocytes are activated following noise exposure, whereas type II fibrocytes are activated following systemic inflammatory stress. Immune-mediated and acoustic trauma-mediated hearing loss syndromes in humans may in part result from the vulnerability of type II and type I fibrocytes to systemic inflammatory stress and acoustic trauma, respectively. Unexpected cell-specific and stress-specific NF-κB activation found in the inner ear in this in vivo study suggest that this approach may have wide applications in demonstrating similar specializations of stress responses in other tissues, including the brain.