MiR‐98‐5p promotes ischemia/reperfusion‐induced microvascular dysfunction by targeting NGF and is a potential biomarker for microvascular reperfusion

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
出处
期刊:Microcirculation [Wiley]
卷期号:28 (1) 被引量:7
标识
DOI:10.1111/micc.12657
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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