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细胞内膜网膜应激阻碍了通过控制关键的外细胞和颗粒细胞分子开关来调节分泌
Mohima Mukherjee1, Chandramouli Mukherjee1, Vinayak Ghosh1
1National Brain Research Centre, Manesar, Gurgaon, Haryana 122052, India.
Journal of cell science
|February 13, 2024
概括
细胞内膜网膜 (ER) 的压力严重损害了神经内分泌细胞中密集核心囊泡 (DCV) 脱细胞. 这种缺陷与eIF2α-ATF4通路有关,影响关键的细胞外调节器.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 密集核心囊泡 (DCVs) 和突触囊泡对于神经元和神经内分泌分泌至关重要.
- 这些囊泡的负载释放功能失调与各种疾病有关.
- 细胞内膜网膜 (ER) 的压力和被破坏的器官通信与疾病的发病有关.
研究的目的:
- 调查ER应激如何影响DCVs调节的外细胞.
- 探索ER和DCV之间的ER压力诱导的交叉语音的功能后果.
主要方法:
- 在PC12神经内分泌细胞中使用thapsigargin和tunicamycin诱导ER压力.
- 在压力和非压力细胞中评估了DCV外细胞.
- 进行了分子分析以确定调节途径,包括ATF4和SNAP25表达.
主要成果:
- 在PC12和INS-1细胞中,ER压力显著抑制了DCV外细胞形成.
- ER压力导致SNAP25表达减少,与ATF4水平增加有关.
- 失去ATF4的功能部分挽救了DCV在应激细胞中的表细胞缺陷.
结论:
- ER压力会导致DCV外细胞形成的严重缺陷.
- eIF2α-ATF4信号轴通过降低基本的外细胞和颗粒生成因子来调节这些缺陷.
- 这突出了一个新的机制,将ER压力与受损的调节分泌联系起来.
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