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过度的甲状腺激素信号诱导小鼠的光感受器退化

Hongwei Ma¹, Fan Yang¹, Lilliana R York¹

¹Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.

|August 18, 2023

概括

过度的甲状腺激素 (TH) 信号破坏视网膜光受体,诱导氧化应激和细胞死亡. 准TH信号可能会在视网膜退行性疾病中保护视力.

科学领域:

眼科医生眼科眼科
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

甲状腺激素 (TH) 信号影响细胞过程,并与视网膜退化有关.
光受体细胞 (棒和) 对于视力至关重要,并且在各种眼睛疾病中发生退化.

研究的目的:

为了研究过度甲状腺激素 (TH) 信号对光受体功能和小鼠模型中的生存的影响.
阐明TH诱导的视网膜损伤背后的分子机制.

主要方法:

小鼠 (C57BL/6,Thra1-/- ,Thrb2-/- ,Thrb-/- ,Nrl-/-) 接受了三甲状腺素 (T3) 的治疗.
评估包括视网膜功能测试,光受体生存/死亡测试 (TUNEL),DNA损伤标志物 (p-γH2AX,8-OHdG),质细胞激活和基因表达分析.
用TH受体 (Thra1,Thrb2) 的遗传删除和抗氧化剂治疗来评估保护作用.

主要成果:

T3处理显著降低了杆和圆光响应,并降低了外核层厚度和圆密度.
在T3治疗的视网膜中观察到氧化应激,DNA损伤和Müller质细胞激活的标志物增加.
基因表达分析揭示了与氧化应激,亡和炎症相关的基因的上调.
删除了Thra1受保护的棒,但没有,而Thrb2删除保留了这两种光受体类型.
抗氧化剂治疗部分保护了光受体,并减少了视网膜应激.

结论:

过度的甲状腺激素 (TH) 信号传递导致光受体通过氧化应激,DNA损伤和亡而退化.
TH信号通路,特别是涉及Thrb2,在光受体生存中发挥着关键作用.
准TH信号通路为保护视网膜退行性疾病中的光受体提供了潜在的治疗策略.

关键词:

这就是为什么我们可以说""是"".鼠标鼠标鼠标鼠标一个光感受器.视网膜视网膜视网膜是一个这是一个棒棒棒棒棒.甲状腺激素是甲状腺激素的一种.

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