piRNA DQ725559通过抑制心肌细胞铁死亡通路抗心肌缺血再灌注损伤的作用  

piRNA DQ725559 Resists Myocardial Ischemia-reperfusion Injury by Inhibiting the Ferroptosis Pathway of Cardiomyocytes

作　　者：王瑞荃 陈鑫哲 王涛[1] 王昆[1] WANG Rui-quan;CHEN Xin-zhe;WANG Tao;WANG Kun(Institute for Translational Medicine,Qingdao University,Qingdao 266021,China)

机构地区：[1]青岛大学转化医学研究院,青岛266021

出　　处：《青岛大学学报（自然科学版）》2024年第1期1-7,共7页Journal of Qingdao University(Natural Science Edition)

基　　金：国家自然科学基金(批准号:82070313)资助。

摘　　要：为探究心肌缺血再灌注损伤(Ischemia-reperfusion Injury,IRI)与铁死亡关系,寻找相关Piwi相互作用RNA(Piwi-interacting RNA,piRNA),利用小鼠乳鼠原代心肌细胞缺氧/复氧(Hypoxia/Reoxygenation,H/R)构建心肌细胞IRI模型,通过细胞生存率反映诱导铁死亡最佳H/R时间点,筛选铁死亡相关piRNA,检测铁死亡相关指标变化。研究结果显示,缺氧18 h/复氧6 h后,心肌细胞铁死亡和IRI呈现关联,抑制DQ725559的表达会加重心肌细胞铁死亡和IRI,过表达DQ725559会减轻心肌细胞铁死亡和IRI。研究结果表明,DQ725559可通过调节心肌细胞铁死亡通路发挥IRI调控作用,过表达DQ725559可成为RNA治疗心血管疾病新策略。To explore the relationship between myocardial ischemia-reperfusion injury(IRI)and ferroptosis,and to find related Piwi-interacting RNA(piRNA),myocardial cell IRI model was constructed by Hypoxia/Reoxygenation(H/R)of primary cardiomyocytes from neonatal mice.The optimal H/R time point for inducing ferroptosis was reflected by cell survival rate.piRNA associated with ferroptosis was screened and changes of ferroptosis related indexes were detected.The results show that ferroptosis is associated with myocardial IRI after hypoxia for 18 h and reoxygenation for 6 h.Inhibition of DQ725559 expression aggravates ferroptosis and myocardial IRI,while overexpression of DQ725559 alleviates ferroptosis and myocardial IRI.This suggests that DQ725559 can play a role in the regulation of myocardial IRI by regulating the ferroptosis pathway of cardiomyocytes,and overexpression of DQ725559 could be a new strategy for RNA therapy of cardiovascular diseases.

关 键 词：缺血再灌注损伤 PIRNA 心肌细胞 铁死亡 

分 类 号：R542.2[医药卫生—心血管疾病]