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乙型肝炎病毒表面蛋白在诱导塞尔托利细胞铁灭菌中的作用

Chengshuang Pan¹, Xiangbin Kong¹, Zhigang Wu²

¹Reproductive Medicine Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

|August 30, 2023

概括

乙型肝炎病毒表面蛋白 (HBs) 通过促进塞尔托利细胞中的铁亡来诱导男性不孕. 这种细胞死亡途径涉及TRIM37介导的谷氨过氧化酶4的抑制,突出了病毒诱导的男性生殖功能障碍的关键机制.

科学领域:

生殖生物学生殖生物学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

乙型肝炎病毒 (HBV) 感染与男性不孕症有关,这种不孕症的特征是精子缺陷.
塞尔托利细胞对于精子生成至关重要,它们的死亡会损害精子质量.
铁,一种受调节的细胞死亡形式,与塞尔托利细胞死亡有关.

研究的目的:

研究暴露于乙型肝炎病毒表面蛋白 (HBs) 的塞尔托利细胞中铁亡的机制.

主要方法:

人类塞尔托利细胞被HBs治疗.
评估了细胞活力,铁亡标志物 (谷氨,马隆迪甲基,Fe2+,脂质过氧化) 和N6-甲基氨酸.
检查的关键蛋白质是:谷氨过氧化酶4 (GPX4),TRIM37,METTL3和IGF2BP2.
使用了qPCR,免疫阻塞,免疫沉和发光测试.

主要成果:

暴露于HBs诱导了塞尔托利细胞中的铁亡,增加了Fe2+并降低了细胞活力和GPX4表达.
HBs显著提高TRIM37的调节,该TRIM37通过ubiquitination抑制了GPX4.
TRIM37静音保护免受HBs诱导的细胞死亡和铁亡.
HBs在TRIM37mRNA上增加了N6-甲基氨酸修饰,通过IGF2BP2.2提高了其稳定性.

结论:

HBs促进塞尔托利细胞铁亡,并通过TRIM37-介导的全方位化对GPX4进行下调,从而降低活力.
TRIM37/GPX4信号通路对于HBV感染的塞尔托利细胞中的铁亡调节至关重要.

关键词:

塞尔托利细胞是什么?在 TRIM3737 中,铁性化 (ferroptosis) 是一种乙型肝炎病毒表面蛋白质B型肝炎病毒表面蛋白质无处不在的化

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