SIRT2通过诱导绵羊细胞中的线粒细胞灭亡来调节细胞灭亡
Xiaohuan Fang1, Wei Xia2, Yatian Qi1
1College of Animal Science and Technology, Hebei Agricultural University, Baoding, 071000, PR China.
Theriogenology
|February 8, 2024
概括
赛尔图因2 (SIRT2) 通过控制线粒细胞灭亡来调节累积细胞的亡. 抑制线粒可以防止细胞亡,而MAPK15在这种SIRT2介导的过程中起着关键作用.
科学领域:
- 生殖生物学 生殖生物学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 累积细胞支持卵细胞的成熟和质量.
- 众所周知,SIRT2 调节了颗粒细胞中的线粒体功能.
- 目前尚不清楚SIRT2在累积细胞内的线粒代谢中的作用.
研究的目的:
- 为了研究SIRT2对绵羊累积细胞中线粒细胞的作用.
- 探索SIRT2通过线粒细胞灭菌影响亡的机制.
- 为了确定SIRT2-mitophagy-apoptosis通路中的潜在关键调节者.
主要方法:
- RNA测序 (RNA-seq) 在SIRT2敲击后识别差异表达基因 (DEG).
- 用线粒抑制剂Mdivi-1.1进行治疗.
- 对亡标记物 (CASP3/CASP9),线粒细胞衰变标记物,水平,细胞染色体C,线粒体形态,ATP水平和mtDNA拷贝数的分析.
- 基因淘汰实验,包括SIRT2和MAPK15的双重淘汰.
主要成果:
- 在线粒体,线粒体和亡途径中,SIRT2敲除丰富的DEGs.
- 线细胞活化显著增加了CASP3/CASP9的表达,而抑制并没有影响亡.
- Mdivi-1预治疗逆转了SIRT2敲击诱导的变化,减少了亡标志物,改善了线粒体功能.
- 双击下SIRT2和MAPK15抵消了SIRT2对线粒和亡的影响.
结论:
- SIRT2通过调节线粒细胞灭亡来调节累积细胞中的亡.
- MAPK15似乎是SIRT2调节的线粒和亡途径中的关键调解者.
- 针对SIRT2-MAPK15-mitophagy轴可能提供改善卵细胞质量的策略.
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