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拼接因子SRSF1通过调节Bcl2L12的替代拼接来减弱心肌细胞的亡

Yilin Xie^1,2, Zhenbo Yang³, Wenxian Chen³

¹Zhuhai People's Hospital (Zhuhai Clinical Medical College of Jinan University), Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Jinan University, Zhuhai, 519000, Guangdong, China.

Cell & bioscience

|November 23, 2024

概括

血清/氨酸拼接因子1 (SRSF1) 通过通过p53通路调节Bcl2L12拼接和亡,防止心脏病发作. 恢复SRSF1可以在心肌梗塞后改善心脏功能.

科学领域:

分子生物学分子生物学
心血管生物学心血管生物学
细胞生物学细胞生物学

背景情况:

异常的替代拼接 (AS) 与病理过程有关.
血清/氨酸剪接因子1 (SRSF1) 改变驱动AS事件.
目前尚不清楚SRSF1在心血管疾病中的作用.

研究的目的:

研究SRSF1在心血管疾病中的功能和机制.
阐明SRSF1在急性心肌梗塞 (AMI) 中的作用.

主要方法:

在AMI小鼠心脏和H9C2细胞中分析SRSF1表达.
在体内研究使用腺相关病毒血清型9用于AMI小鼠SRSF1过度表达.
RNA测序 (RNA-seq) 用于识别由SRSF1.1调节的AS事件.
研究SRSF1对Bcl2L12剪接的影响及其与p53.3的相互作用.

主要成果:

在AMI小鼠心脏和H2O2处理的H9C2细胞中,SRSF1的表达显著降低.
在体内SRSF1过度表达改善了AMI小鼠的心脏功能,并减少了心脏病发作的大小.
SRSF1 调节了 Bcl2L12 的替代拼接,特别影响了 7 号外子的包含.
沉默SRSF1导致Bcl2L12的切断,损害了它与p53的相互作用,并促进了亡.

结论:

SRSF1 作为一个关键的拼接因子,调节 Bcl2L12 拼接切换.
通过p53通路,SRSF1具有抗亡作用.
针对SRSF1-介导的拼接,通过减轻心肌细胞亡,为心血管疾病提供了潜在的治疗策略.

关键词:

另一个替代拼接方法.细胞灭亡 (apoptosis) 是一种死亡的过程.Bcl2L1212 的使用情况心肌梗塞的心脏病发作在SRSF1中,我们可以使用SRSF1.

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