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Kidney Week

Abstract: PO0397

circBNC2 Inhibits Renal Fibrosis Through Regulating G2/M Cell Cycle Transition

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • 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

Emerging evidence indicates that AKI is a causative factor for subsequent development of chronic kidney disease (CKD). G2/M cell cycle arrest of TECs promotes AKI to CKD progression, but the regulation of G2/M cell cycle arrest of TECs is largely unclear. Circular RNAs (circRNAs), a class of noncoding RNA, are recently found to be dysregulated in tubular epithelial cells (TECs) during renal ischemia/reperfusion (I/R) injury. However, the effects and underlying mechanisms of circRNAs in the progression of renal fibrosis are largely unrevealed.


Mild-AKI (20 min- IRI) and severe-AKI (40 min-IRI) were performed in C57BL/6 mice. The expression of circRNA were analyzed in the freshly isolated tubules from these mice by RNA-seq. One of the dysregulated circRNA, circBNC2 were identified and analyzed by Northern blot, FISH and real-time qPCR in HK2 cells, mouse primary TECs and in mouse kidney. HK-2 cells were exposed to hypoxia as in vitro model. To study the function of circBNC2, we used the CRISPR-Cas9 genome editing system to specifically knocked out circBNC2 in HK2, while circBNC2 was overexpression by plasmid. To study the function of circBNC2 in vivo, we applied adeno-associated virus (AAV)-based circBNC2 overexpression in C57BL/6 mice 3 weeks before performing IRI model. G2/M cell cycle arrest and pro-fibrotic cytokine expression were evaluated in HK2 and primary TECs. Renal fibrosis was evaluated in mouse kidney sections.


The un-biased sequencing showed significant down-regulation of circBNC2 in TECs from severe-IRI mice, as compared to the TECs from mild-IRI mice and control mice. Knockout circBNC2 in HK2 and primary TECs led to G2/M cell cycle arrest and pro-fibrotic cytokines expression. While overexpression of circBNC2 decreased hypoxia-induced G2/M cell cycle arrest of TECs. Preventative overexpression of circBNC2 in vivo ameliorated 40 min-IRI induced renal fibrosis.


Our results showed that circBNC2 regulated G2/M cell cycle transition of TECs and might be served as a therapeutic target for AKI-progressed CKD.


  • Government Support – Non-U.S.