Abstract
ObjectiveLong noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is increased under the condition of ischemia. This study intended to identify the mechanism of TUG1 in renal ischemia-reperfusion (I/R).MethodsFirst, a rat model of acute renal injury induced by I/R was established, followed by the measurement of blood urea nitrogen (BUN), serum creatine (SCr), methylenedioxyphetamine (MDA) and superoxide dismutase (SOD) in the serum of rats. TUG1 was knocked down in I/R rats (ko-TUG1 group). Next, histological staining was used to evaluate the pathological damage and apoptosis of rat kidney. Western blot analysis was used to detect the levels of apoptosis- and autophagy-related proteins and transmission electron microscope was used to observe autophagosomes. Autophagy and apoptosis were evaluated after inhibition of the autophagy pathway using the inhibitor 3-MA. The targeting relation among TUG1, microRNA (miR)-29 and phosphatase and tensin homolog (PTEN) were validated. Lastly, the effects of TUG1 on biological behaviors of renal tubular cells were evaluated in vitro.ResultsIn vivo, the levels of BUN, SCr and MDA in the serum of I/R-treated rats were increased while SOD level and autophagosomes were reduced, tubule epithelial cells were necrotic, and TUG1 was upregulated in renal tissues of I/R-treated rats, which were all reversed in rats in the ko-TUG1 group. Autophagy inhibition (ko-TUG1 + 3-MA group) averted the protective effect of TUG1 knockdown on I/R-treated rats. TUG1 could competitively bind to miR-29 to promote PTEN expression. In vitro, silencing TUG1 (sh-TUG1 group) promoted viability and autophagy of renal tubular cells and inhibited apoptosis.ConclusionsLncRNA TUG can promote PTEN expression by competitively binding to miR-29 to promote autophagy and inhibited apoptosis, thus aggravating acute renal injury in I/R-treated rats.
Highlights
As a major cause of most cardiovascular diseases, ischemia/reperfusion (I/R) injury is recognized as a process when the blood supply returns to tissues after hypoxia, which causes ischemia and induces a cascade of events associated with oxidative damage and dysfunction [1]
taurine upregulated gene 1 (TUG1) is upregulated in renal I/R-treated rats The levels of serum blood urea nitrogen (BUN), serum creatine (SCr), MDA and superoxide dismutase (SOD) were measured in the sham group and I/R group
We detected the expression of TUG1 in the renal tissues of the two groups by Reverse transcription quantitative polymerase chain reaction (RT-qPCR)
Summary
As a major cause of most cardiovascular diseases, ischemia/reperfusion (I/R) injury is recognized as a process when the blood supply returns to tissues after hypoxia, which causes ischemia and induces a cascade of events associated with oxidative damage and dysfunction [1]. Serious clinical manifestations such as acute heart failure, myocardial infarction, cerebral and gastrointestinal disorder, systemic inflammatory response and multiple organ dysfunctions are critical medical conditions of I/R injury [2]. Tubular cells are critical targets of I/R injury in renal transplantation [6]. If the biomarkers or targeted therapeutic interventions are to be explored, it is urgent to first comprehend the mechanism of renal tubular cells in response to I/R
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