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SGK1通过PI3K/SGK1/Wnt信号通路调解简单疹角膜炎

Wei Ye¹, Songyi Tang¹, Yue Wang¹

¹Medical School, Nanjing University, Nanjing 210093, China; Department of Ophthalmology, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.

Cellular signalling

|December 14, 2024

概括

简单疹角膜炎 (HSK) 涉及眼部的HSV-1感染. 这项研究表明,PI3K激活SGK1,促进病毒复制和亡,确定SGK1是HSK的关键治疗标.

科学领域:

眼科医生眼科眼科
病毒学病毒学
分子生物学分子生物学

背景情况:

简单疹病毒1型 (HSV-1) 导致简单疹角膜炎 (HSK),是导致视力丧失的主要原因.
目前针对HSK的抗病毒治疗有局限性,包括耐药性和仅在活跃病毒复制期间的有效性.
角膜上皮细胞 (CEC) 中的HSV-1感染的分子机制需要进一步阐明,以确定新的治疗点.

研究的目的:

调查酸丁醇3'-激酶 (PI3K) 和血清和葡萄糖皮质体调节蛋白激酶1 (SGK1) 在角膜上皮细胞 (CEC) 内的HSV-1感染中的作用.
探索涉及PI3K,SGK1和Wnt/β-catenin信号传递的分子途径,在HSV-1诱导的亡和复制的背景下.
评估SGK1作为治疗HSK的潜在治疗标.

主要方法:

使用全转录组测序,定量实时聚合酶链反应 (RT-qPCR) 和免疫光染色来评估病毒载量和基因表达.
用SGK1 (GSK 650394) 和PI3K (LY294002) 的抑制剂来研究通路调节.
西部涂抹,流细胞测量和细胞内西部涂抹被用来分析蛋白质表达,亡和病毒复制.

主要成果:

在人类角膜上皮细胞 (HCECs) 和BALB/c小鼠中,HSV-1感染增加了病毒载量和亡.
在HSV-1感染的HCEC和角膜组织中,SGK1的表达被上调.
抑制SGK1或PI3K降低了HSV-1复制,SGK1和β-catenin表达和CEC亡,表明PI3K/SGK1通路激活及其通过Wnt/β-catenin通路促进病毒复制和亡的作用.

结论:

在CEC中,在HSV-1感染期间,PI3K/SGK1信号通路被激活.
由PI3K驱动的升级SGK1,促进HSV-1复制并诱导CEC亡,部分通过Wnt/β-catenin通路.
SGK1代表了治疗简单疹角膜炎 (HSK) 的有希望的治疗标.

关键词:

在GSK650394中使用.希腊银行 (HSK) 是一个.在HSV-1病毒中,在PI3K中,PI3K是指PI3K.一个SGK1的SGK1.他们不想做.

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