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13 January 2020 : Animal Research

[Retracted] 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

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

SELECT DATE(`ARTICLE_DATE`.`DATE_MAIN`) AS `dat`, `JOUR_WWW_ARTICLES`.`ID_ARTICLE` FROM `JOUR_WWW_ARTICLES` INNER JOIN `ARTICLE_DATE` ON (`JOUR_WWW_ARTICLES`.`ID_ARTICLE` = `ARTICLE_DATE`.`ICID`) WHERE `ARTICLE_DATE`.`ID_DATE_KIND` = 5 AND `JOUR_WWW_ARTICLES`.`ID_PARENT_ARTICLE` =
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13 January 2020 : Animal Research

[Retracted] 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

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

SELECT DATE(`ARTICLE_DATE`.`DATE_MAIN`) AS `dat`, `JOUR_WWW_ARTICLES`.`ID_ARTICLE` FROM `JOUR_WWW_ARTICLES` INNER JOIN `ARTICLE_DATE` ON (`JOUR_WWW_ARTICLES`.`ID_ARTICLE` = `ARTICLE_DATE`.`ICID`) WHERE `ARTICLE_DATE`.`ID_DATE_KIND` = 5 AND `JOUR_WWW_ARTICLES`.`ID_PARENT_ARTICLE` =
You have an error in your SQL syntax; check the manual that corresponds to your MySQL server version for the right syntax to use near '' at line 9
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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750