ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

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

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: SA-PO343

Wnt/β-Catenin-Promoted Macrophage Proliferation, Migration, and Alternative Activation Contribute to Kidney Fibrosis

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 308 CKD: Mechanisms of Tubulointerstitial Fibrosis

Authors

  • Feng, Ye, Nanjing medical university, Nanjing, Jiangsu, China
  • Dai, Chunsun, Nanjing medical university, Nanjing, Jiangsu, China
Background

The Wnt/β-catenin pathway initiates a signaling cascade that is crucial in both normal development and throughout life. However, the role and mechanisms for Wnt/β-catenin in regulating macrophage activation and its contribution to kidney fibrosis remain to be determined.

Methods

A mouse model with with tamoxifen-inducible deletion of β-catenin in macrophages was created.

Results

Here we found that in addition to promoting macrophage proliferation and migration, Wnt/β-catenin could exacerbate IL4 or TGFβ1-induced macrophage M2 polarization via activating STAT3 molecule. This observation was further confirmed in a mouse model with inducible deletion of β-catenin in macrophages. In that model, kidney fibrosis, macrophage accumulation, proliferation and M2 polarization were all diminished in the fibrotic kidneys compared to their control littermates.

Conclusion

This study demonstrated that Wntb-catenin signaling activation promotes kidney fibrosis may be ascribed to stimulating macrophage proliferation, migration, and M2 polarization.

Funding

  • Government Support - Non-U.S.