超氧化物脱酶2缺乏与小鼠中加强的中央化学反应有关:对呼吸调节的影响
Esteban Díaz-Jara1, Katherine Pereyra1, Sinay Vicencio1
1Laboratory of Cardiorespiratory Control, Pontificia Universidad Católica de Chile, Santiago, Chile.
Redox biology
|December 24, 2023
概括
在Retrotrapezoid核 (RTN) 中降低的超氧化物转化酶2 (SOD2) 增加了超氧化物离子水平,增加了中央化学反射驱动和改变呼吸模式. 这突显了SOD2在呼吸控制中的作用.
科学领域:
- 神经科学是一个神经科学.
- 呼吸系统生理学 呼吸系统生理学
- 氧化压力生物学 氧化压力生物学
背景情况:
- 中央化学受体调节呼吸,其中Retrotrapezoid核 (RTN) 是一个关键区域.
- 在RTN中的高超氧化 (O2.-) 水平与增强的中央化学反应相关.
- 超氧化物脱酶2 (SOD2) 缺乏与各种疾病有关,但其在RTN化学接收中的作用尚不清楚.
研究的目的:
- 调查部分SOD2删除对RTN中的O2-积累的影响.
- 评估SOD2缺乏对中央呼吸道化学反射功能和呼吸模式的影响.
- 确定SOD2在RTN中的细胞局部.
主要方法:
- 在异构体SOD2淘汰赛 (SOD2+/-) 和野生类型 (WT) 小鼠中进行全身囊造影.
- 在RTN部分和孤立的线粒体中测量O2.-水平.
- 评估SOD2蛋白表达,RNA测序和免疫光染色.
主要成果:
- 在RTN中,SOD2+/-小鼠显示SOD2水平降低,O2增加,以及线粒体功能障碍.
- 在SOD2+/-小鼠中,呼吸系统对高头的反应加剧,呼吸模式发生变化.
- SOD2局部存在于RTN星体细胞中,而不是化学受体神经元,在SOD2+/-星体细胞中观察到形态变化.
结论:
- SOD2在RTN中调节O2.-水平,影响中央化学反射功能的作用.
- 减少SOD2表达可能导致RTN O2.-增加,导致化学反应驱动和呼吸改变.
- SOD2的调节失调以及脑干呼吸区域的随后的O2-增加会扰乱呼吸控制,导致氧化应激相关疾病的呼吸功能障碍.
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