University of Oulu

Wang, L., Mohanasundaram, P., Lindström, M., Asghar, M. N., Sultana, G., Misiorek, J. O., Jiu, Y., Chen, H., Chen, Z., Toivola, D. M., Cheng, F., & Eriksson, J. E. (2022). Vimentin suppresses inflammation and tumorigenesis in the mouse intestine. Frontiers in Cell and Developmental Biology, 10.

Vimentin suppresses inflammation and tumorigenesis in the mouse intestine

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Author: Wang, Linglu1; Mohanasundaram, Ponnuswamy2; Lindström, Michelle2;
Organizations: 1School of Pharmaceutical Sciences (Shenzhen), Shenzhen Campus of Sun Yat-sen University, Shenzhen, China
2Cell Biology, Biosciences, Faculty of Science and Engineering, Åbo Akademi University, Turku, Finland
3Department of Molecular Neurooncology, Institute of Bioorganic Chemistry Polish Academy of Sciences, Poznan, Poland
4Key Laboratory of Molecular Virology and Immunology, The Center for Microbes, Development and Health, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China
5University of Chinese Academy of Sciences, Beijing, China
6Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland
7Turku Center for Disease Modeling, University of Turku, Turku, Finland
8InFLAMES Research Flagship Center, Åbo Akademi University, Turku, Finland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 3.1 MB)
Persistent link:
Language: English
Published: Frontiers Media, 2022
Publish Date: 2022-09-08


Vimentin has been implicated in wound healing, inflammation, and cancer, but its functional contribution to intestinal diseases is poorly understood. To study how vimentin is involved during tissue injury and repair of simple epithelium, we induced colonic epithelial cell damage in the vimentin null (Vim−/−) mouse model. Vim−/− mice challenged with dextran sodium sulfate (DSS) had worse colitis manifestations than wild-type (WT) mice. Vim−/− colons also produced more reactive oxygen and nitrogen species, possibly contributing to the pathogenesis of gut inflammation and tumorigenesis than in WT mice. We subsequently describe that CD11b+ macrophages served as the mainly cellular source of reactive oxygen species (ROS) production via vimentin-ROS-pSTAT3–interleukin-6 inflammatory pathways. Further, we demonstrated that Vim−/− mice did not develop colitis-associated cancer model upon DSS treatment spontaneously but increased tumor numbers and size in the distal colon in the azoxymethane/DSS model comparing with WT mice. Thus, vimentin has a crucial role in protection from colitis induction and tumorigenesis of the colon.

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Series: Frontiers in cell and developmental biology
ISSN: 2296-634X
ISSN-E: 2296-634X
ISSN-L: 2296-634X
Volume: 10
Article number: 862237
DOI: 10.3389/fcell.2022.862237
Type of Publication: A1 Journal article – refereed
Field of Science: 1182 Biochemistry, cell and molecular biology
Funding: This research was supported by Academy of Finland 315139/332582; Sigrid Juselius Foundation, ÅAU Center of Excellence of Cellular Mechanostasis, EuroCellNet COST Action (CA15214); InFLAMES Flagship Programme of the Academy of Finland (decision number: 337531); European Union Framework 7 International Reintegration Grant, Åbo Akademi University Center of Excellence on Cell Stress and Molecular Aging to DT, and Turku Doctoral Programme for Biomedical Sciences to JOM and MA, the National Natural Science Foundation of China (81702750, 81970145, and 82001698); the National Natural Science Foundation of China (81970145 and 82001698); Natural Science Foundation of Guangdong Province (2020A1515011465 and 2020A151501467, China); Science, Technology and Innovation Commission of Shenzhen Municipality (JCYJ20190807151609464, JCYJ20200109142605909, and JCYJ20210324120007020, China); Sun Yat-sen University (20ykzd17, China); International Collaboration of Science and Technology of Guangdong Province (2020A0505100031, China); Guangdong Provincial Key Laboratory of Digestive Cancer Research (No. 2021B1212040006, China).
Dataset Reference: The Supplementary Material for this article can be found online at:
Copyright information: © 2022 Wang, Mohanasundaram, Lindström, Asghar, Sultana, Misiorek, Jiu, Chen, Chen, Toivola, Cheng and Eriksson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.