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13 January 2020 : Animal Research

[Retracted: 18 Jan 2022] The Nephroprotective Effect of TNF Receptor-Associated Factor 6 (TRAF6) Blockade on LPS-Induced Acute Renal Injury Through the Inhibition if Inflammation and Oxidative Stress

Xuemei Chen1ABCD, Yiqing Zhao1BD, Jiajun Xu2AEFG, Jiachun Bao1BD, Junyao Zhao1CE, Jingfeng Chen1CD, Guowei Chen2EF, Jibo Han2ACEFG*

DOI: 10.12659/MSM.919698

Med Sci Monit 2020; 26:e919698

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Xuemei Chen, Yiqing Zhao, Jiajun Xu, Jiachun Bao, Junyao Zhao, Jingfeng Chen, Guowei Chen, Jibo Han. The Nephroprotective Effect of TNF Receptor-Associated Factor 6 (TRAF6) Blockade on LPS-Induced Acute Renal Injury Through the Inhibition if Inflammation and Oxidative Stress. Med Sci Monit, 2020; 26: e919698. DOI: 10.12659/MSM.919698

Abstract

BACKGROUND: Inflammation and oxidative stress play important roles in the pathogenesis of acute kidney injury (AKI). TRAF6 functions as a signal transducer in the Toll-like receptor 4 signaling pathway. Several reports have previously implicated TRAF6 signaling in kidney pathology. Here, we investigated whether TRAF6 blockade can mitigate inflammatory responses and oxidative stress in AKI.

MATERIAL AND METHODS: C57BL/6 mice were injected with lipopolysaccharide (LPS, 15 mg/kg) to induce AKI. Double immunofluorescence staining of kidney tissues showed that TRAF6 was localized to renal tubular epithelial cells, and then a tubular epithelial cell line (NRK-52E) was used for in vitro analysis. TRAF6 was blocked in vitro using siRNA and in vivo using AAV2/2 shRNA.

RESULTS: The knockdown of TRAF6 in mice by AAV2-shTRAF6 significantly reduced renal inflammation, oxidative stress, apoptosis and kidney dysfunction in AKI. In vitro, silencing the expression of TRAF6 attenuated LPS(0.5 μg/mL)-induced inflammatory responses and oxidative stress and upregulated proapoptotic factors. Furthermore, the beneficial actions of TRAF6 blockade were closely associated with its ability to increase IκB-α and Nrf2.

CONCLUSIONS: Our findings provide direct evidence that TRAF6 mediates LPS-induced inflammation and oxidative stress, leading to renal dysfunction. We also show that TRAF6 inhibition is a potential therapeutic option to prevent AKI.

Keywords: Retracted Publication

Retraction note

Med Sci Monit 2022; 28:e936124     https://medscimonit.com/abstract/index/idArt/936124
 
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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750