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SP1/ADAM10/DRP1轴链接平滑肌细胞和内皮细胞之间的细胞间通信在低氧肺高血压下

Hongyan Li¹, Yi Liu¹, Xianbao Shi¹

¹Department of Respiratory Disease, The First Affiliated Hospital, Jinzhou Medical University, Jinzhou 121000, China.

Biochimica et biophysica acta. Molecular basis of disease

|February 16, 2025

概括

SP1在内皮细胞中调节ADAM10,推动光滑肌肉细胞的增殖,并导致肺高血压缺氧. 抑制ADAM10或其下游通路 (DRP1,PI3K/AKT/mTOR) 可以减轻这些影响.

科学领域:

心血管生物学心血管生物学
细胞信号传输细胞信号传输
肺高血压研究肺高血压研究

背景情况:

内皮细胞 (ECs) 和光滑肌细胞 (SMCs) 的交叉是低氧肺高血压 (HPH) 的关键.
了解调解这种交叉的分子机制对于HPH治疗至关重要.

研究的目的:

研究SP1/ADAM10/DRP1和ADAM10-PI3K-AKT-mTOR信号在HPH中EC-SMC交叉声中的作用.
确定ADAM10是否在低氧条件下调解EC对SMC的影响.

主要方法:

在接受过氧治疗的老鼠和EC中评估ADAM10表达.
在EC中利用了ADAM10的淘汰和过度表达.
检查了EC调节介质对SMC增殖和亡的影响.
在SMC中分析了下游信号通路 (DRP1,PI3K/AKT/mTOR).
研究了ADAM10.的SP1规则.

主要成果:

在缺氧时ADAM10的表达增加,其降低缓解了HPH和缺氧诱导的EC功能障碍.
条件介质从低氧ECs促进了SMC增殖和减少了细胞亡,ADAM10敲击减轻了效应.
在EC中的ADAM10通过DRP1和PI3K/AKT/mTOR通路影响了SMC.
SP1被确定为ADAM10表达的调节者.

结论:

在低氧诱导的EC中,SP1增强了ADAM10分泌.
由ECs释放的ADAM10通过DRP1和PI3K/AKT/mTOR信号驱动SMC的恶性表型,有助于HPH的进展.

关键词:

亚当10 亚当10 亚当 DRP1 DRP1 的使用方法内皮细胞内皮细胞的内皮细胞.在HPH中,HPH是HPH.SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 顺滑肌肉细胞是什么?

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