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SOX9 枯竭通过阻断 ERK/p38 信号传递来减轻视网膜质细胞铁亡

Wei Wei¹, Yufeng Zhang¹, Langen Li¹

¹Ophthalmology Department, Inner Mongolia Autonomous Region People's Hospital, Hohhot 010017, Inner Mongolia Autonomous Region, China.

|February 9, 2024

概括

抑制SOX9通过通过ERK/p38通路减少氧化应激,炎症和铁亡,从而保护视网膜缺血-再输损伤,提供潜在的青光眼治疗.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

视网膜缺血-反 (I/R) 损伤是全球不可逆转失明的重要原因之一.
了解导致视网膜I/R损伤的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

调查SOX9在视网膜I/R损伤中的调节作用.
阐明SOX9影响视网膜I/R损伤的潜在机制.

主要方法:

使用661W细胞建立了体内视网膜I/R损伤模型和体内氧气-葡萄糖剥夺/氧化恢复 (OGD/R) 模型.
评估了组织学变化,SOX9表达,细胞因子产生,乳酸脱酶 (LDH),氧化应激标志物 (ROS,脂质ROS) 和铁亡标志物.
利用西部斑块进行蛋白质表达分析和ERK信号激动剂 (LM22B-10) 探索机械路径.

主要成果:

在视网膜I / R损伤中,SOX9被发现在体内和体外都受到上调.
在661W细胞中,SOX9敲击证明了对OGD/R诱导的氧化应激,炎症和铁亡的保护作用.
在OGD/R后观察到ERK/p38信号激活,被SOX9淘汰抑制;ERK激动剂部分逆转了SOX9淘汰的保护作用.

结论:

抑制SOX9可以通过阻断氧化应激,炎症和铁亡来减轻视网膜I / R损伤.
通过SOX9抑制,ERK/p38信号的失活是防止视网膜I/R损伤的关键机制.
向SOX9代表了一种潜在的治疗策略,用于预防视网膜I/R损伤和减轻青光眼.

关键词:

在ERK的信号传输中.铁化是铁化的一种.眼光障碍眼光障碍眼光障碍眼光障碍这就是SOX9的SOX9.

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