LncRNA NEAT1 promotes hypoxia‐induced renal tubular epithelial apoptosis through downregulating miR‐27a‐3p

Abstract

Acute kidney injury (AKI) is a common kidney disorder that affects public health and the incidence of AKI. Sepsis, acute ischemia or hypoxia is the main reason for the occurrence of AKI. Recently, noncoding RNA that include microRNA and long noncoding RNA (lncRNAs) were reported to play important roles in AKI as well as have the potential to serve as a biomarker or therapeutic target for the development of the diagnostic and prognostic strategies of AKI. In the current study, we aimed to investigate the expression and biological function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in ischemia‐induced AKI in patients' sample and in vitro. The expressions of NEAT1 and miR‐27a‐3p in ischemia/reperfusion‐induced AKI patients were examined by quantitative reverse transcription polymerase chain reaction. Cell injury was induced by treatment of human kidney tubular cells (HK‐2) with CoCl2. After treatment, the influences of NEAT1 and miR‐27a‐3p on the cell apoptosis in the CoCl2‐stimulated HK‐2 were tested by flow cytometry. The flow analysis results showed that the expression of NEAT1 was markedly higher in the ischemia‐induced AKI patients compared with normal control. Moreover, repression the expression of NEAT1 decreased CoCl2‐induced injury in HK‐2. The expression of miR‐27a‐3p was negatively regulated by NEAT1. Inhibition the expression of NEAT1 attenuated overexpression of miR‐27a‐3p enhanced CoCl2‐induced injury. In summary, an ischemia‐induced injury may be enhanced by a high level of NEAT1 through targeting miR‐27a‐3p. Thus, NEAT1 has the potential to be explored as a biomarker for diagnosis and target for therapeutic strategies in ischemia‐induced AKI.

NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p

“…A previous study suggested that lncRNA NEAT1 contributed to sepsis-triggered AKI via repressing miR-204 and activating the NF-κB pathway [19]. Besides, Jiang et al revealed that NEAT1 aggravated ischemiainduced injury via functioning as a ceRNA of miR-27a-3p [9]. Similar to previous research studies, the NEAT1 expression was dramatically increased in patients with sepsis in comparison with healthy controls.…”

“…LncRNA nuclear-enriched abundant transcript 1 (NEAT1) has been reported to play a crucial role in the innate immune response. Previous research has corroborated that NEAT1 aggravated ischemiainduced AKI via directly targeting miR-27a-3p [9]. Moreover, NEAT1 promoted sepsis-induced brain injury in mice by mediating the nuclear factor (NF)-κB pathway [10].…”

LncRNA CYTOR attenuates sepsis‐induced myocardial injury via regulating miR‐24/XIAP

“…37 And in sepsisinduced organ injury, interaction between lncRNA and miRNA also plays an important role. For instance, lncRNA NEAT1 promotes hypoxia-induced renal tubular epithelial apoptosis via downregulating miR-27a-3p 38 ; lncRNA MALAT1 aggravates cardiac inflammation and dysfunction in sepsis by regulating miR-125b and p38 MAPK/NF-κB pathway. 39 Our data indicated that CYTOR could inhibit miR-24 expression by binding with it to attenuate the injury of cardiomyocytes during sepsis.…”

Knockdown of lncRNA NEAT1 suppresses hypoxia-induced migration, invasion and glycolysis in anaplastic thyroid carcinoma cells through regulation of miR-206 and miR-599

“…Zheng et al underscored that hypoxia induced NEAT1 expression in hepatocellular carcinoma (HCC), and NEAT1 silencing repressed HCC cell migration and invasion under hypoxia [28]. Jiang et al highlighted that NEAT1 accelerated hypoxia-induced renal tubular epithelial apoptosis via down-regulating miR-27a-3p [29].…”