miR-223 improves intestinal inflammation through inhibiting the IL-6/STAT3 signaling pathway in dextran sodium sulfate-induced experimental colitis
© 2020 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd..
INTRODUCTION: The pathogenesis of inflammatory bowel disease (IBD) has not yet been clarified and is closely related to several pro-inflammatory factors. MicroRNA-233 (miR-223) might be involved in the development of IBD; however, the mechanism underlying its pathogenesis is unclear. In this study, we attempted to determine the role of miR-223 in dextran sodium sulfate (DSS)-induced colitis and explore the involvement of the IL-6/STAT3 pathway in the development of intestinal mucosal inflammation.
MATERIALS AND METHODS: Except control (WT) group, male C57BL/6 mice were provided DSS, then treated for with miR-223 agomir or antagomir including DSS group, DSS + miR-223 agomir (DSS + A) group, and DSS + miR-223 antagomir (DSS + AN) group. The colitis symptoms were observed, the disease activity index (DAI) score were recorded daily, and colonic inflammation was evaluated by histopathological scoring. The expression of myeloperoxidase (MPO), cytokines and IL-6/STAT3 pathway-related proteins were measured.
RESULTS: miR-223 expression in the terminal ileum and colon was increased in the DSS group compared with the WT group. Colitis symptoms were significantly alleviated in the DSS + A group and exacerbated in the DSS + AN group after administration of the miR-223 agomir and antagomir, respectively. MPO, tumor necrosis factor-α, IL-6, and IL-17 were decreased and IL-10 was increased in the DSS + A group, but these changes were reversed in the DSS + AN group. Gp130, p-STAT3, Bcl-2, and Bcl-xl in the colon declined in the DSS + A group, but these levels increased in the DSS + AN group.
CONCLUSIONS: The upregulation of miR-223 by agomir administration alleviated colonic inflammation in a DSS-induced colitis model, which was likely mediated by inhibiting the production of pro-inflammatory cytokines via the IL-6/STAT3 signaling pathway. These findings provide evidence that miR-223 might have potential therapeutic implications in IBD.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:9 |
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| Enthalten in: |
Immunity, inflammation and disease - 9(2021), 1 vom: 01. März, Seite 319-327 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhang, Juanjuan [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 15.10.2021 Date Revised 15.10.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1002/iid3.395 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM318977664 |
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| 100 | 1 | |a Zhang, Juanjuan |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a miR-223 improves intestinal inflammation through inhibiting the IL-6/STAT3 signaling pathway in dextran sodium sulfate-induced experimental colitis |
| 264 | 1 | |c 2021 | |
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| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2020 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. | ||
| 520 | |a INTRODUCTION: The pathogenesis of inflammatory bowel disease (IBD) has not yet been clarified and is closely related to several pro-inflammatory factors. MicroRNA-233 (miR-223) might be involved in the development of IBD; however, the mechanism underlying its pathogenesis is unclear. In this study, we attempted to determine the role of miR-223 in dextran sodium sulfate (DSS)-induced colitis and explore the involvement of the IL-6/STAT3 pathway in the development of intestinal mucosal inflammation | ||
| 520 | |a MATERIALS AND METHODS: Except control (WT) group, male C57BL/6 mice were provided DSS, then treated for with miR-223 agomir or antagomir including DSS group, DSS + miR-223 agomir (DSS + A) group, and DSS + miR-223 antagomir (DSS + AN) group. The colitis symptoms were observed, the disease activity index (DAI) score were recorded daily, and colonic inflammation was evaluated by histopathological scoring. The expression of myeloperoxidase (MPO), cytokines and IL-6/STAT3 pathway-related proteins were measured | ||
| 520 | |a RESULTS: miR-223 expression in the terminal ileum and colon was increased in the DSS group compared with the WT group. Colitis symptoms were significantly alleviated in the DSS + A group and exacerbated in the DSS + AN group after administration of the miR-223 agomir and antagomir, respectively. MPO, tumor necrosis factor-α, IL-6, and IL-17 were decreased and IL-10 was increased in the DSS + A group, but these changes were reversed in the DSS + AN group. Gp130, p-STAT3, Bcl-2, and Bcl-xl in the colon declined in the DSS + A group, but these levels increased in the DSS + AN group | ||
| 520 | |a CONCLUSIONS: The upregulation of miR-223 by agomir administration alleviated colonic inflammation in a DSS-induced colitis model, which was likely mediated by inhibiting the production of pro-inflammatory cytokines via the IL-6/STAT3 signaling pathway. These findings provide evidence that miR-223 might have potential therapeutic implications in IBD | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a IL-6/STAT3 signaling pathway | |
| 650 | 4 | |a cytokines | |
| 650 | 4 | |a dextran sodium sulfate-induced colitis | |
| 650 | 4 | |a inflammatory bowel disease | |
| 650 | 4 | |a miR-223 | |
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| 650 | 7 | |a MIRN223 microRNA, mouse |2 NLM | |
| 650 | 7 | |a MicroRNAs |2 NLM | |
| 650 | 7 | |a Sulfates |2 NLM | |
| 650 | 7 | |a sodium sulfate |2 NLM | |
| 650 | 7 | |a 0YPR65R21J |2 NLM | |
| 650 | 7 | |a Dextran Sulfate |2 NLM | |
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| 700 | 1 | |a Guo, Zhen |e verfasserin |4 aut | |
| 700 | 1 | |a Da, Binlin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhu, Weiming |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Qiurong |e verfasserin |4 aut | |
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