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抑制 Dad1 诱导心肌细胞死亡,通过削弱细胞粘附,从而导致心肌细胞死亡

Shota Mori¹, Rumi Kimura¹, Hirofumi Morihara^1,2

¹Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Suita City, Japan.

American journal of physiology. Cell physiology

|November 29, 2024

概括

对细胞死亡的防御者1 (Dad1) 敲击导致心肌细胞死亡,通过损害整合素N-糖化和细胞粘附. Dad1对于维持心脏平衡和预防心脏衰竭至关重要.

科学领域:

心血管生物学心血管生物学
细胞死亡机制细胞死亡机制
蛋白质糖基化蛋白质的糖基化.

背景情况:

心肌细胞损失是心力衰竭的关键驱动因素.
抑制心肌细胞死亡是一个潜在的治疗策略.
防御细胞死亡1 (Dad1) 在心肌细胞中的作用尚不清楚.

研究的目的:

研究 Dad1 在心肌细胞存活和功能中的作用.
阐明 Dad1 影响心肌细胞死亡的分子机制.
探索针对心力衰竭的 Dad1 的治疗潜力.

主要方法:

补充DNA微阵列和siRNA查以确定心肌细胞死亡的调节者.
在新生小鼠心肌细胞 (NRCMs) 中,siRNA介导的 Dad1 的淘汰.
评估细胞活力,细胞亡标志物 (切割的caspase-3),细胞扩散,肌纤维生成,整合素的N-糖化和焦粘附激酶 (FAK) 活性.
研究了Oligosaccharyltransferase (OST) 复合体内Dad1和Stt3A之间的相互作用.

主要成果:

Dad1的敲击降低了NRCM的生存能力和诱导的亡,独立于ER的压力.
爸爸1的敲击损害了细胞的扩散和肌纤维形成,这表明无.
Dad1的敲击破坏了整合素α5和β1的N-糖化,导致FAK的失活.
增强细胞粘附减弱了 Dad1 敲击诱导的心肌细胞死亡.
Dad1 和 Stt3A 在 OST 综合体内相互稳定.

结论:

Dad1通过调节整合素N-糖化和细胞粘附来维持心肌细胞生存至关重要.
Dad1通过保护整合素功能和下游信号传导,在抑制阿诺基斯方面发挥着关键作用.
Dad1通过整合素的翻译后修饰,促进心脏平衡,为心脏的OST复合体功能提供了新的见解.

关键词:

在N-glycosylation的过程中.心肌细胞的死亡.细胞粘附细胞粘附防御细胞死亡的防御者 1 细胞死亡 1 整体的整体是整体的

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