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Open Access

Foodborne toxin Aflatoxin B1 induced glomerular podocyte inflammation through proteolysis of RelA, downregulation of miR-9 and CXCR4/TXNIP/NLRP3 pathway

Jie Zhanga,b,, Shuang Yangb, Baocai Xuc, Zihui Qinc,d, Xinyi Guoc,d, Ben Weic,d, Qinghua Wue,f, Kamil Kucae, Tushuai Lig,h( ), Wenda Wuc,d,e( )
School of Biology and Food Engineering, Changshu Institute of Technology, Suzhou 215500, China
Center for Clinical Mass Spectrometry, School of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China
MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China
Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Kralove 50003, Czech Republic
College of Life Science, Yangtze University, Jingzhou 434025, China
Wuxi Medical College, Jiangnan University, Wuxi 214122, China
Wuxi Translational Medicine Research Center and Jiangsu Translational Medicine Research Institute Wuxi Branch, Wuxi 214013, China

Peer review under responsibility of Tsinghua University Press.

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Highlights

• AFB1 induced murine kidney disfunction and glomerular podocyte inflammation;

• AFB1-induced RelA ubiquitin-proteasome degradation brought about downregulation of miR-9;

• miR-9 low-expression to upregulate CXCR4 was sufficient to induce podocyte inflammation through increase of TXNIP to initiate NLRP3 inflammasome activation in response to AFB1 exposure.

Graphical Abstract

Abstract

Aflatoxin B1 (AFB1) is a naturally-occurring mycotoxin and recognized as the most toxic foodborne toxin, particularly causing damages to kidney. Glomerular podocytes are terminally differentiated epithelial cells. AFB1 induces podocyte inflammation, proteinuria and renal dysfunction. Studying the mechanism of AFB1-induced podocyte inflammation and murine kidney dysfunction, we detected that AFB1 increased ubiquitin-dependent degradation of the transcription factor RelA through enhanced interaction of RelA with E3 ubiquitin ligase tripartite motif containing 7 (TRIM7) in mouse podocyte clone-5 (MPC-5) and mouse glomeruli. Reduction of RelA resulted in decreasing microRNA-9 (miR-9) and activating the chemokine receptor 4 (CXCR4), thioredoxin interacting protein (TXNIP), and NOD-like receptor pyrin domain-containing 3 (NLRP3) signaling axis (CXCR4/TXNIP/NLRP3 pathway), leading to podocyte inflammation. We also determined that downregulation of miR-9 led to CXCR4 expression and the downstream TXNIP/NLRP3 pathway activation. Overexpression of miR-9 or deletion of CXCR4 suppressed AFB1-induced CXCR4/TXNIP/NLRP3 pathway, resulting in alleviating podocyte inflammation and kidney dysfunction. Our findings indicated that ubiquitin-dependent proteolysis of RelA, downregulation of miR-9, and activation of CXCR4/TXNIP/NLRP3 pathway played an essential role in AFB1-induced glomerular podocyte inflammation. Our study revealed a novel mechanism, via RelA, for the control of AFB1’s nephrotoxicity, leading to an effective protection of food safety and public health.

Keywords

miRNA-9Chemokine (C-X-C motif) receptor 4RelA ubiquitin-dependent degradationAfl atoxin B1Podocyte infl ammation

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Food Science and Human Wellness
Volume 13 Issue 4,
July 2024
Pages 2289-2309
DOI: 10.26599/FSHW.2022.9250191
Cite this article:
Zhang J, Yang S, Xu B, et al. Foodborne toxin Aflatoxin B1 induced glomerular podocyte inflammation through proteolysis of RelA, downregulation of miR-9 and CXCR4/TXNIP/NLRP3 pathway. Food Science and Human Wellness, 2024, 13(4): 2289-2309. https://doi.org/10.26599/FSHW.2022.9250191

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Received: 14 February 2023
Revised: 09 April 2023
Accepted: 12 May 2023
Published: 20 May 2024
© 2024 Beijing Academy of Food Sciences. Publishing services by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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