MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL
Many microRNAs (miRNAs) are selectively expressed in mammalian immune cells and have been linked to immune responses in host defense and autoimmune disease. In macrophages, miRNAs regulate cell metabolism by repressing the expression of genes such as transcription factors, enzymes, and metabolism-re...
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| Format: | Article |
| Language: | English |
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Hindawi Limited
2023-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2023/2457006 |
| _version_ | 1797777959283589120 |
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| author | Young Jun Kang |
| author_facet | Young Jun Kang |
| author_sort | Young Jun Kang |
| collection | DOAJ |
| description | Many microRNAs (miRNAs) are selectively expressed in mammalian immune cells and have been linked to immune responses in host defense and autoimmune disease. In macrophages, miRNAs regulate cell metabolism by repressing the expression of genes such as transcription factors, enzymes, and metabolism-related molecules, as well as the expression of genes that impact inflammatory responses and phenotype determination. Previous studies showed that miR-22 plays a role in a variety of biological processes, such as cancer cell growth, cell survival, and cell expansion. In CD4 + T cells of inflammatory bowel disease patients, miR-22 is upregulated and regulates inflammasome-mediated responses. However, it has not yet been determined how miR-22 contributes to the activation of innate immune cells. In this study, we identified a mechanism of toll-like receptors- (TLR-) dependent miR-22 induction that regulates the downstream signaling pathway linking inflammatory responses and macrophage polarization. MiR-22 is induced via TLR-signaling, which regulates the induction of Slc2a1 (glucose transporter 1 and Glut1) and Tnfsf9 (tumor necrosis factor 9, 4-1BB ligand, and 4-1BBL) mRNAs that contribute to sustained inflammatory responses and the polarization of macrophages. Our observations support further efforts to explore a potential therapeutic strategy using miR-22 for the modulation of excessive macrophage activation for the treatment of inflammatory diseases. |
| first_indexed | 2024-03-12T23:10:29Z |
| format | Article |
| id | doaj.art-577d08cdc2bc46fbb47d7a4db6bd62be |
| institution | Directory Open Access Journal |
| issn | 2314-7156 |
| language | English |
| last_indexed | 2024-03-12T23:10:29Z |
| publishDate | 2023-01-01 |
| publisher | Hindawi Limited |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj.art-577d08cdc2bc46fbb47d7a4db6bd62be2023-07-18T05:00:02ZengHindawi LimitedJournal of Immunology Research2314-71562023-01-01202310.1155/2023/2457006MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBLYoung Jun Kang0Molecular Medicine Research InstituteMany microRNAs (miRNAs) are selectively expressed in mammalian immune cells and have been linked to immune responses in host defense and autoimmune disease. In macrophages, miRNAs regulate cell metabolism by repressing the expression of genes such as transcription factors, enzymes, and metabolism-related molecules, as well as the expression of genes that impact inflammatory responses and phenotype determination. Previous studies showed that miR-22 plays a role in a variety of biological processes, such as cancer cell growth, cell survival, and cell expansion. In CD4 + T cells of inflammatory bowel disease patients, miR-22 is upregulated and regulates inflammasome-mediated responses. However, it has not yet been determined how miR-22 contributes to the activation of innate immune cells. In this study, we identified a mechanism of toll-like receptors- (TLR-) dependent miR-22 induction that regulates the downstream signaling pathway linking inflammatory responses and macrophage polarization. MiR-22 is induced via TLR-signaling, which regulates the induction of Slc2a1 (glucose transporter 1 and Glut1) and Tnfsf9 (tumor necrosis factor 9, 4-1BB ligand, and 4-1BBL) mRNAs that contribute to sustained inflammatory responses and the polarization of macrophages. Our observations support further efforts to explore a potential therapeutic strategy using miR-22 for the modulation of excessive macrophage activation for the treatment of inflammatory diseases.http://dx.doi.org/10.1155/2023/2457006 |
| spellingShingle | Young Jun Kang MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL Journal of Immunology Research |
| title | MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL |
| title_full | MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL |
| title_fullStr | MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL |
| title_full_unstemmed | MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL |
| title_short | MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL |
| title_sort | microrna 22 regulates the pro inflammatory responses and m1 polarization of macrophages by targeting glut1 and 4 1bbl |
| url | http://dx.doi.org/10.1155/2023/2457006 |
| work_keys_str_mv | AT youngjunkang microrna22regulatestheproinflammatoryresponsesandm1polarizationofmacrophagesbytargetingglut1and41bbl |