Nagashima Reiko, Sugiyama Chie, Yoneyama Masanori, Kuramoto Nobuyuki, Kawada Koichi, Ogita Kiyokazu
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, 45-1 Nagaotoge-cho, Hirakata, Osaka 573-0101, Japan.
Neurochem Int. 2007 Jul-Sep;51(2-4):209-15. doi: 10.1016/j.neuint.2007.04.023. Epub 2007 May 7.
Glutamate-cysteine ligase (GCL), previously known as gamma-glutamylcysteine synthetase, is the rate-limiting enzyme for GSH synthesis. The expression of GCL is mediated by activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB), which are known to participate in stress-induced apoptotic pathways in neuronal cells. In this study, we investigated the changes in the level of these transcription factors as well as of GCL catalytic subunit in the cochlea in response to acoustic overstimulation. Nuclear extracts were prepared from the cochlear at various time points after intense noise exposure (4kHz octave band, 125dB sound pressure level, 5h), and then determined DNA binding activity of the transcription factors. AP-1 DNA binding was markedly increased 2-12h after the noise exposure, with a peak at 2h after the exposure. NF-kappaB DNA binding was also increased immediately after the exposure. Semi-quantitative RT-PCR revealed that the catalytic subunit of GCL mRNA was elevated in the cochlea 2-24h post the exposure. Further immunohistochemical study revealed that increased level of GCL catalytic subunit observed at least in the spiral ganglion cells after the exposure. These results suggest that intense noise exposure facilitates the expression of GCL catalytic subunit in the cochlea possibly through the activation of transcription factors including AP-1 and NF-kappaB.
谷氨酸-半胱氨酸连接酶(GCL),以前称为γ-谷氨酰半胱氨酸合成酶,是谷胱甘肽(GSH)合成的限速酶。GCL的表达由激活蛋白-1(AP-1)和核因子-κB(NF-κB)介导,已知它们参与神经元细胞应激诱导的凋亡途径。在本研究中,我们调查了在受到声学过度刺激后,耳蜗中这些转录因子以及GCL催化亚基水平的变化。在强烈噪声暴露(4kHz倍频程,125dB声压级,5小时)后的不同时间点从耳蜗制备核提取物,然后测定转录因子的DNA结合活性。噪声暴露后2-12小时,AP-1 DNA结合显著增加,暴露后2小时达到峰值。暴露后立即NF-κB DNA结合也增加。半定量RT-PCR显示,暴露后2-24小时耳蜗中GCL mRNA的催化亚基升高。进一步的免疫组织化学研究显示,暴露后至少在螺旋神经节细胞中观察到GCL催化亚基水平增加。这些结果表明,强烈噪声暴露可能通过激活包括AP-1和NF-κB在内的转录因子促进耳蜗中GCL催化亚基的表达。