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

Abstract: SA-PO237

Tripartite Motif-Containing 55 (TRIM55) Participates in the Immune Response in Experimental Anti-Thy1 Glomerulonephritis

Session Information

  • Glomerular: Cell Biology
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Glomerular

  • 1003 Glomerular: Cell Biology

Authors

  • Chen, Lei, First Affiliated Hospital of Medicine School, Xi'an Jiaotong University, XI'an, Shannxi, China
  • Jiang, Hongli, Dialysis Center of First Affiliated Hospital of Medicine School, Xi?an Jiaotong University,, Xi'an,Shaanxi,, China
Background

Mesangial proliferative glomerulonephritis (MsPGN) is considered as an immune-related disease. Its pathogenesis is involved with activation of mesangial cells and the subsequent immune inflammatory response. However, the mechanism underlying the regulation of immune response remains largely elusive.Tripartite motif family was reported to be closely related to immune regulation. In this study, we performed a series of experiments in vivo and vitro to investigate the role of tripartite motif-containing 55 (TRIM55), a member of tripartite motif family, in the progression of MsPGN.

Methods

36 male SD rats were randomly divided into 6 groups, 5 of which were received tail vein injection of anti Thy-1 antibody (2.5 mg/kg body weight), and the remaining group was received PBS injection as negative control(NC). Specimens of the NC group were collected at 0d after the injection, while those of other groups were collected at 1d, 2d, 3d, 4d,and 5d, respectively. Immunohistochemical stainig of CD68 was performed to evaluate the level of macrophages infiltration. qPCR analysis of glomerulus was performed to examine the expression of TRIM55 . Primary RMCs with overexpression of TRIM55 were obtained through plasmid transfection. In addition, si-RNA tranfection was used to knock down the expression of TRIM55 in primary RMCs. qPCR analysis was conducted to detect the level of cytokines, such as TNF-α, CCL2, CXCL6, CXCL10, and IL-6.

Results

PAS staining results indicated mesangial dissolution occurred since 1d, followed by inflammatory cell infiltration. CD68 immunohistochemical staining results showed that macrophages infiltration peaked at 1d and then decreased gradually. The expression of TRIM55 mRNA also peaked at 1d and decreased gradually, which was consistent with the trend of macrophages infiltration. In primary RMCs, knockdown of DBP led to down-regulation of the expression of cytokines (TNF-α, CCL2, CXCL6, CXCL10 and IL-6). On the other hand, the expression of those cytokines(TNF-α, CCL2, CXCL6, CXCL10 and IL-6) significantly increased in TRIM55-overexpressed primary RMCs.

Conclusion

The above results indicate that TRIM55 participates in the immune response in anti-Thy1 nephritis by regulating the production of cytokines. We duce TRIM55 may be a promising therapeutic intervention to ameliorate leukocyte infiltration in MsPGN.