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心脏缩中的DNA损伤和核形态变化是由SNRK通过actin脱聚合介导的

Paulina Stanczyk^1,2,3, Yuki Tatekoshi^1,3, Jason S Shapiro^1,3

¹Division of Cardiology, Department of Medicine, and Feinberg Cardiovascular and Renal Research Institute, Northwestern University School of Medicine, Chicago, IL, USA.

bioRxiv : the preprint server for biology

|July 28, 2023

概括

与SNF1相关的激酶 (SNRK) 调节心肌细胞的核结构和DNA损伤反应 (DDR). 由于SNRK的损失会破坏actin聚合和核形态,导致心脏缩恶化,这表明SNRK/DSTN相互作用是治疗标.

科学领域:

心血管生物学心血管生物学
分子心脏病学分子心脏病学
细胞和核动力学

背景情况:

适当的核组织对于心肌细胞功能和心血管健康至关重要.
异常的核形态和染色质结构与心血管疾病的进展有关.
在心脏缩中,DNA损伤反应 (DDR) 的作用尚未完全理解.

研究的目的:

研究SNF1相关激酶 (SNRK) 在心脏缩和DDR中的作用.
确定SNRK是否影响心肌细胞核结构和功能.
为了确定SNRK参与心脏重塑的分子点.

主要方法:

使用心脏特异性的SNRK淘汰赛小鼠接受了跨大动脉带带 (TAC).
在体外进行调节SNRK表达和评估核参数的研究.
采用蛋白组学来识别SNRK目标和共同免疫沉来确认DSTN相互作用.

主要成果:

由于SNRK缺乏,心脏缩和TAC后功能障碍加剧,DDR标志物增加.
在实验室中,SNRK的破坏导致了DNA损伤,染色质的紧缩,并改变了核的形状.
确定了Destrin (DSTN) 作为SNRK目标;SNRK-DSTN相互作用调节了actin聚合,核形态和DDR.

结论:

在缓解心脏缩和DNA损伤方面,SNRK起着至关重要的作用.
SNRK与DSTN相互作用,调节actin动态,从而保持心肌细胞的核完整性.
准SNRK/DSTN通路为压力过载引起的心脏缩提供了潜在的治疗策略.

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