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Kidney Week

Abstract: PO0415

Long Noncoding RNA Neat1 Promotes Tubular Epithelial Cells Apoptosis to Facilitate the Progression of AKI to CKD

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Ma, Tongtong, Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China
  • Wang, Peng, Division of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Guangzhou, China

The severity and frequency of acute kidney injury (AKI) determine if the injury leads to chronic kidney disease (CKD). A growing number of research shows that the injury of tubular epithelial cells (TECs) is the driving force during chronic progression of AKI. However, there are limited knowledge about the role of lncRNAs in the progression of AKI.


To screen out the candidate lncRNA in the progression of AKI to CKD, 8-week old C57BL/6 mice were subjected to mild-AKI (20 min-ischemic reperfusion injury) and severe-AKI (40 min- ischemic reperfusion injury). RNA-sequencing was performed with the isolated tubules from mild- or severe- AKI mouse. The expression of a candidate lncRNA Neat1 was evaluated by FISH, Northern blot and real-time qRT-PCR in HK2 cells and mouse kidney tissues. To study the biological function of Neat1 in vitro, CRISPR-Cas9 was used to knock out Neat1, while Neat1 was ectopic overexpressed by lentivirus. HK2 cells were cultured in anoxic environment as the in vitro model to study the function of Neat1. RNA pull down was performed to screen out the microRNAs that bound to Neat1. Knocking down Neat1 in vivo was performed by injecting Adeno-associated virus serotype 9 (AAV9) particles carrying siRNA targeting Neat1. Flow cytometer was used to calculate the apoptotic cells under each treatment. TUNEL was applied to evaluated the apoptotic TECs in kidney sections.


The expression of Neat1 was upregulated in the tubules from severe AKI mouse, as compared to mild AKI mouse. Knocking out Neat1 inhibited hypoxia-induced HK2 cells apoptosis while overexpression of Neat1 enhanced the apoptosis of HK2 cells in vitro. Furthermore, knockdown of Neat1 in vivo reduced the apoptosis of TECs and improved the kidney functions of IRI mice.


Our results showed that LncRNA neat1 regulated apoptosis of TECs and might be served as a therapeutic target to ameliorate AKI.


  • Government Support – Non-U.S.