ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2019 and some content may be unavailable. To unlock all content for 2019, please visit the archives.

Abstract: SA-PO941

Genetic or Pharmacologic Blockade of Enhancer of Zeste Homolog 2 Inhibits the Progression of Peritoneal Fibrosis

Session Information

Category: Dialysis

  • 703 Dialysis: Peritoneal Dialysis

Authors

  • Liu, Na, shanghai east hospital, Shanghai, China
  • Shi, Yingfeng, Nephrology department Shanghai Dongfang Hospital, Shanghai, SHANGHAI, China
  • Qiu, Andong, Tongji University, Shanghai, SHANGHAI, China
  • Zhuang, Shougang, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island, United States
Background

Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in many cancers. However, the role of EZH2 in peritoneal fibrosis remains unknown.

Methods

We investigated EZH2 expression in peritoneal dialysis (PD) patients and assessed its role in peritoneal fibrosis induced by chlorhexidine gluconate (CG) or high glucose peritoneal dialysis fluid (PDF) in mice by using 3-deazaneplanocin A (3-DZNeP), and EZH2 conditional knockout mice in fibroblasts.

Results

An abundance of EZH2 was detected in the peritoneum of patients with PD associated peritonitis and the dialysis effluent of long-term PD patients. EZH2 was also highly expressed in the peritoneum of mice after injury by CG or PDF, and treatment with 3-DZNeP attenuated peritoneal fibrosis and inhibited activation of several pro-fibrotic mechanisms. Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced matrix metalloproteinases-2 (MMP-2) and MMP-9 expression. Finally, EZH2-KO mice exhibited less peritoneal fibrosis compared with EZH2-WT mice. In cultured peritoneal mesothelial cells, EZH2 inhibition resulted in suppression of α-SMA and Collagen I and preservation of E-cadherin.

Conclusion

These results indicate that EZH2 is a key epigenetic regulator that promotes peritoneal fibrosis. Targeting EZH2 may have the potential to prevent and treat peritoneal fibrosis.