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Abstract: FR-PO421

Inhibitor of Growth 2 Regulates the High Glucose Induced Cell Cycle Arrest and Epithelial-to-Mesenchymal Transition in HK-2 Cells

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic


  • Xin, Wei, Shandong Provincial Hospital affiliated to Shandong University, Jinan, China
  • Yan, Ruijuan, Shandong Provincial Qianfoshan Hospital affiliated to Shandong University, Jinan, China
  • Ma, Yuan, Shandong University, Ji'Nan, Shandong, China
  • Lv, Tingting, Shandong University, Ji'Nan, Shandong, China
  • Chen, Liyong, Shandong Provincial Hospital affiliated to Shandong University, Jinan, China
  • Wan, Qiang, Shandong Provincial Qianfoshan Hospital affiliated to Shandong University, Jinan, China

Cell cycle dysregulation has been linked to various kidney injuries in recent years; however, its involvement in the fibrosis of diabetic kidney disease (DKD) is far from being clarified. ING2 (inhibitor of growth 2) is the second member of the inhibitor of growth family and participates in the regulation of many cellular processes, yet the role of ING2 in the process of DKD remains largely unknown. In the present study, we aimed to investigate the involvement of ING2 in the cell cycle arrest and epithelial-to-mesenchymal transition (EMT) process in diabetic conditions and the underlying mechanism for it.


The human proximal tubular epithelial cells (HK-2) were stimulated with high glucose and diabetic mice were generated by streptozotocin injection. ING2 expression was detected by western blotting and immunofluorescent staining in vitro and immunohistochemistry staining in vivo. The expression of ING2 was silenced by siRNA transfection. Cell proliferation was analyzed by CCK-8 and EdU assay. Cell cycle arrest was measured by flow cytometry. The EMT markers were detected by qPCR and western blotting. The p53 activation by high glucose was proved by chromatin immunoprecipitation (ChIP) and the downstream p21 expression was detected by qPCR and western blotting.


We first revealed that the expression of ING2 was increased both in diabetic mouse kidney in vivo and in high glucose stimulated HK-2 cells in vitro. ING2 downregulation ameliorated the reduced proliferation and cell cycle arrest induced by high glucose in HK-2 cells. Moreover, p53 was activated under hyperglycemia condition and ING2 knockdown suppressed p21 expression by reducing p53 acetylation and finally alleviated the expression of EMT markers in the high glucose stimulated HK-2 cells.


Our study demonstrated that cell cycle regulation is bound up with the EMT of high glucose cultured HK-2 cells, suggesting a novel function of ING2 as a potential therapeutic strategy targeting cell cycle arrest for the kidney fibrosis in DKD.