通过光滑肌肉细胞的表型转变,NUPR1调节肺栓塞进展
Shu Wang1, Aizhen Xu1, Maoqing Chen1
1Department of Respiratory and Critical Care Medicine, Zibo Central Hospital, Zibo, Shandong, 255036, China.
Heliyon
|November 11, 2024
概括
核蛋白1 (NUPR1) 通过促进肺动脉光滑肌细胞 (PASMC) 增殖和表型转变,加剧肺栓塞 (PE). 减少NUPR1表达改善了PE模型中的肺病理.
科学领域:
- 心血管研究研究心血管研究
- 细胞生物学 细胞生物学
- 肺部医学 肺部医学
背景情况:
- 肺栓塞 (PE) 是一种严重的病症,其特征是肺动脉阻塞.
- 肺动脉光滑肌细胞 (PASMCs) 在PE期间在血管重塑中发挥关键作用.
- 驱动PASMC在PE中的表型转换的特定分子机制需要进一步阐明.
研究的目的:
- 调查核蛋白1 (NUPR1) 在肺栓塞 (PE) 病变发生过程中的作用.
- 确定NUPR1对肺动脉光滑肌细胞 (PASMCs) 现型变化的影响.
主要方法:
- 通过自身肺栓塞输液建立了小鼠PE模型.
- 在肺组织和PASMC中使用免疫光和西部斑分析评估NUPR1表达.
- 在PE大鼠和PASMC中使用了NUPR1敲击和过度表达的lentiviral载体.
- 在正常和缺氧条件下分析了PASMC表型标记,增殖,入侵和迁移.
主要成果:
- 在人类的PASMC中,NUPR1的表达升高,在小鼠PE肺部显著增加.
- 在PE大鼠中,NUPR1敲击改善了肺损伤,而过度表达加剧了肺损伤.
- 低氧诱导了老鼠PASMC中的NUPR1逐渐上调.
- 过度表达NUPR1促进了PASMC表型转变到合成表型,增强了扩散,入侵和迁移.
结论:
- 在PE中NUPR1表达升高通过促进它们的表型转变,加剧了异常的PASMC增殖.
- 在PE的病态进展中,NUPR1起到关键的调解作用.
- 准NUPR1可能为治疗肺栓塞提供治疗策略.
更多相关视频
相关概念视频
Nitric Oxide Signaling Pathway
4.9K
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
4.9K
Intracellular Signaling Affects Focal Adhesions
2.6K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
2.6K


