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Tisp40 deficiency limits renal inflammation and promotes tubular cell proliferation in renal ischemia reperfusion injury.

Authors :
Qin C
Li M
Bai T
Yang K
Xu T
Zhang J
Source :
Experimental cell research [Exp Cell Res] 2018 Oct 01; Vol. 371 (1), pp. 255-261. Date of Electronic Publication: 2018 Aug 17.
Publication Year :
2018

Abstract

Renal ischemia reperfusion (IR) is a common cause of acute kidney injury (AKI), and no effective treatment is available to date. In our previous studies, we demonstrated that Tisp40 exacerbates tubular cell apoptosis and tubulointerstitial fibrosis after renal IR injury. However, the role of Tisp40 in renal inflammatory responses and tubular cell proliferation during renal IR injury remains unknown. In this study, Tisp40 knockout (KO) and wild-type (WT) mice were induced with or without renal IR injury. For renal IR, bilateral renal pedicels were exposed and clamped to induce 30 min of ischemia. After 48 h of reperfusion, the kidneys were collected for analyses. Results showed that Tisp40 deficiency attenuates neutrophil and macrophage infiltration after renal IR. Consistently, the protein levels of TNF-α and MCP-1 were markedly decreased, and the phosphorylation levels of IκBα and P65 were inhibited in Tisp40-deficient mice than in WT mice in renal IR injury. In addition, compared with WT mice, Tisp40 deficiency significantly increased the expression levels of proliferative cellular nuclear antigen and phosphorylated Erk1/2 after renal IR injury. In conclusion, Tisp40 deficiency limits renal inflammatory responses and promotes tubular cell proliferation in ischemic AKI.<br /> (Copyright © 2018 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1090-2422
Volume :
371
Issue :
1
Database :
MEDLINE
Journal :
Experimental cell research
Publication Type :
Academic Journal
Accession number :
30121191
Full Text :
https://doi.org/10.1016/j.yexcr.2018.08.019