相关实验视频

Updated: Jan 17, 2026

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

Published on: May 23, 2025

miR-140-3p通过MAP2K6/p38路径缓解肺动脉平滑肌细胞功能障碍

Ling Chen^1,2, Jia-Yi Zhang¹, Lei Huang¹

¹Department of Pulmonary & Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.

Journal of biochemical and molecular toxicology

|September 23, 2025

概括

在肺动脉高血压 (PAH) 中,microRNA-140-3p的下调. 恢复miR-140-3p水平可以抑制PASMC的扩散,缓解PAH,从而揭示出一种新的治疗标.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
基因规则基因规则

背景情况:

肺动脉高血压 (PAH) 涉及由肺动脉光滑肌细胞 (PASMC) 增殖和亡抵抗驱动的肺血管重塑.
微RNAs (miRNAs) 参与细胞增殖和细胞亡,但miR-140-3p在PAH中的作用尚未被探索.

研究的目的:

调查miR-140-3p在肺动脉高血压 (PAH) 病变发生中的作用.
阐明 miR-140-3p 在 PASMC 中的功能背后的分子机制.

主要方法:

在SU5416/缺氧 (SuHx) 诱导的PAH模型和缺氧治疗的人类PASMC中评估miR-140-3p表达.
在体内使用miR-140-3p agomir,在体内使用miR-140-3p模仿剂/抑制剂.
进行了双露西法酶记者测定,以确定miR-140-3p目标.
分析了下游的信号通路,包括MAP2K6,p38,MMP2/9,Bcl2和BAX.

主要成果:

在PAH模型和低氧治疗的PASMC中,miR-140-3p的表达显著下调.
miR-140-3p agomir的使用改善了PAH症状,包括右心室缩压和血管重塑.
miR-140-3p抑制了缺氧诱导的PASMC增殖和迁移,同时促进了亡.
miR-140-3p直接向MAP2K6,抑制MAP2K6/p38通路并影响MMP2/9和Bcl2/BAX的表达.

结论:

miR-140-3p通过抑制PASMC增殖和促进亡,在PAH中起着保护作用.
该miR-140-3p/MAP2K6/p38信号轴是PAH病原发生的关键调节机制.
miR-140-3p代表了治疗肺动脉高血压的有希望的治疗标.

关键词:

缺氧缺氧是指缺氧的情况.这是一个微型RNA.肺动脉高血压肺动脉高血压肺动脉平滑肌肉细胞肺动脉的细胞

更多相关视频

Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses

Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses

Published on: June 8, 2022

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Published on: October 19, 2013

相关概念视频

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...