Open AccessLncRNA TUG1 attenuates ischaemia‐reperfusion‐induced apoptosis of renal tubular epithelial cells by sponging miR‐144‐3p via targeting Nrf2
Author(s) -
Zhao Sheng,
Chen Wu,
Li Wei,
Yu Weimin,
Li Siqi,
Rao Ting,
Ruan Yuan,
Zhou Xiangjun,
Liu Cong,
Qi Yucheng,
Cheng Fan
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16924
Subject(s) - oxidative stress , apoptosis , microrna , downregulation and upregulation , renal ischemia , kidney , in vitro , hypoxia (environmental) , acute kidney injury , renal injury , biology , ischemia , reperfusion injury , pharmacology , chemistry , medicine , biochemistry , endocrinology , gene , organic chemistry , oxygen
Renal ischaemia/reperfusion (I/R) injury may induce kidney damage and dysfunction, in which oxidative stress and apoptosis play important roles. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are reported to be closely related to renal I/R, but the specific molecular mechanism is still unclear. The purpose of this research was to explore the regulatory effect of lncRNA TUG1 on oxidative stress and apoptosis in renal I/R injury. This research revealed that in renal I/R injury and hypoxia/reperfusion (H/R) injury in vitro, the expression level of lncRNA TUG1 was upregulated, and oxidative stress levels and apoptosis levels were negatively correlated with the expression level of lncRNA TUG1. Using bioinformatics databases such as TargetScan and microRNA.org, microRNA‐144‐3p (miR‐144‐3p) was predicted to be involved in the association between lncRNA TUG1 and Nrf2. This study confirmed that the level of miR‐144‐3p was significantly reduced following renal I/R injury and H/R injury in vitro, and miR‐144‐3p was determined to target Nrf2 and inhibit its expression. In addition, lncRNA TUG1 can reduce the inhibitory effect of miR‐144‐3p on Nrf2 by sponging miR‐144‐3p. In summary, our research shows that lncRNA TUG1 regulates oxidative stress and apoptosis during renal I/R injury through the miR‐144‐3p/Nrf2 axis, which may be a new treatment target for renal I/R injury.