医学
TRPV1型
微循环
再灌注损伤
拮抗剂
神经生长因子
缺血
体内
心脏病学
内科学
心肌梗塞
生物标志物
受体
细胞培养
瞬时受体电位通道
转染
生物
生物技术
生物化学
遗传学
作者
Yisen Hu,Jingjie Xiong,Hao Wen,Heng Wei,Xiaocong Zeng
摘要
Abstract Objective This study examined the correlation between serum miR‐98‐5p levels and indices of microvascular reperfusion in patients undergoing primary percutaneous coronary intervention (pPCI) after ST‐segment elevation myocardial infarction (STEMI). Additionally, we evaluated the mechanisms by which miR‐98‐5p promoted ischemia/reperfusion (I/R)‐induced injury in both cultured cell lines and an animal model. Methods Circulating miR‐98‐5p levels were measured and compared from 171 STEMI patients undergoing pPCI, who were divided into two groups: no‐reflow and reflow. The levels of miR‐98‐5p, nerve growth factor (NGF), and transient receptor potential vanilloid 1 (TRPV1) were analyzed in cultured human coronary endothelial cells (HCECs) exposed to hypoxia/reoxygenation (H/R). The effects of antagomir‐98‐5p on myocardial I/R‐induced microvascular dysfunction in vivo were evaluated. Target gene expression and activity were assessed. Results Higher miR‐98‐5p levels were associated with compromised indices of microvascular reperfusion. In vitro experiments on HCECs showed that exposure to H/R significantly increased miR‐98‐5p levels. We identified NGF as a novel target of miR‐98‐5p. Further, antagomir‐98‐5p relieved microvascular dysfunction and enhanced the expression of NGF and TRPV1 in the rat myocardial I/R model. Conclusions MiR‐98‐5p promotes microvascular dysfunction by targeting the NGF‐TRPV1 axis. Serum miR‐98‐5p serves as a potential biomarker for microvascular reperfusion.
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