Open Access

CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs

  • Authors:
    • Wenjing Xian
    • Jiali Wu
    • Qingshu Li
    • Xunsong Du
    • Na Wang
    • Daiyu Chen
    • Wuxi Gao
    • Jun Cao
  • View Affiliations

  • Published online on: May 28, 2021     https://doi.org/10.3892/mmr.2021.12180
  • Article Number: 541
  • Copyright: © Xian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Increasing evidence has demonstrated that regulatory T cells (Tregs) suppress innate immunity, as well as protect the kidneys from ischemia‑reperfusion injury (IRI) and offer a potentially effective strategy to prevent or alleviate renal IRI. The present study explored whether C‑X‑C motif chemokine receptor 3 (CXCR3) alleviated renal IRI by increasing Tregs. Male C57BL/6J mice were divided into sham‑surgery, IRI, CXCR3 overexpression (OE‑CXCR3)+IRI, PC61+IRI and OE‑CXCR3+PC61+IRI groups. Histopathological examination of the kidney was carried out using hematoxylin‑eosin and Masson staining. The levels of serum creatinine (Scr) and blood urea nitrogen (BUN) were measured. Blood and kidney levels of IL‑6, TNF‑α, C‑C motif chemokine ligand (CCL)‑2 and IL‑10 were detected by ELISA and western blotting. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px) and malondialdehyde (MDA) in kidney tissues were also measured to assess oxidative stress. The population of Tregs in the kidney was assessed using flow cytometry. The results demonstrated that administration of OE‑CXCR3 to IRI mice significantly decreased the levels of Scr, BUN, IL‑6, TNF‑α, CCL‑2 and MDA, increased the levels of IL‑10, SOD and GSH‑Px, and mitigated the morphologic injury and fibrosis induced by IR compared with the IRI group. In addition, administration of OE‑CXCR3 induced significant reductions in the expression levels of fibrosis‑related markers, including fibronectin and type IV collagen, and increased the number of Tregs. These roles of OE‑CXCR3 were significantly neutralized following deletion of Tregs with PC61 (anti‑CD25 antibody). Together, the present study demonstrated that injection of OE‑CXCR3 lentiviral vectors into animal models can alleviate renal IRI by increasing the number of Tregs. The results may be a promising approach for the treatment of renal IRI.
View Figures
View References

Related Articles

Journal Cover

July-2021
Volume 24 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Xian W, Wu J, Li Q, Du X, Wang N, Chen D, Gao W and Cao J: CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs. Mol Med Rep 24: 541, 2021.
APA
Xian, W., Wu, J., Li, Q., Du, X., Wang, N., Chen, D. ... Cao, J. (2021). CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs. Molecular Medicine Reports, 24, 541. https://doi.org/10.3892/mmr.2021.12180
MLA
Xian, W., Wu, J., Li, Q., Du, X., Wang, N., Chen, D., Gao, W., Cao, J."CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs". Molecular Medicine Reports 24.1 (2021): 541.
Chicago
Xian, W., Wu, J., Li, Q., Du, X., Wang, N., Chen, D., Gao, W., Cao, J."CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs". Molecular Medicine Reports 24, no. 1 (2021): 541. https://doi.org/10.3892/mmr.2021.12180