E3 ubiquitin ligase COP1-mediated CEBPB ubiquitination regulates the inflammatory response of macrophages in sepsis-induced myocardial injury
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature..
CCAAT/enhancer-binding protein beta (CEBPB) has been associated with sepsis. However, its role in sepsis-induced myocardial injury (SIMI) remains ill-defined. This research was designed to illustrate the involvement of CEBPB in SIMI and its upstream modifier. The transcriptomic changes in heart biopsies of mice that had undergone polymicrobial sepsis were downloaded from the GEO dataset for KEGG enrichment analysis. CEBPB, on the TNF signaling pathway, was significantly enhanced in the myocardial tissues of mice with SIMI. Downregulation of CEBPB alleviated SIMI, as evidenced by minor myocardial injury and inflammatory manifestations. Moreover, ubiquitination modification of CEBPB by constitutive photomorphogenesis protein 1 homolog (COP1) led to the degradation of CEBPB and inhibited inflammatory responses in macrophages. Upregulation of COP1 protected against SIMI in mice overexpressing CEBPB. Collectively, our findings demonstrated that COP1 protected the heart against SIMI through the ubiquitination modification of CEBPB, which might be a novel therapeutic approach in the future.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:35 |
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| Enthalten in: |
Mammalian genome : official journal of the International Mammalian Genome Society - 35(2024), 1 vom: 01. Feb., Seite 56-67 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yu, Yangzi [VerfasserIn] |
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| Links: |
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| Themen: |
Arabidopsis Proteins |
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| Anmerkungen: |
Date Completed 23.02.2024 Date Revised 23.02.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s00335-023-10027-y |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM364718269 |
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| 520 | |a CCAAT/enhancer-binding protein beta (CEBPB) has been associated with sepsis. However, its role in sepsis-induced myocardial injury (SIMI) remains ill-defined. This research was designed to illustrate the involvement of CEBPB in SIMI and its upstream modifier. The transcriptomic changes in heart biopsies of mice that had undergone polymicrobial sepsis were downloaded from the GEO dataset for KEGG enrichment analysis. CEBPB, on the TNF signaling pathway, was significantly enhanced in the myocardial tissues of mice with SIMI. Downregulation of CEBPB alleviated SIMI, as evidenced by minor myocardial injury and inflammatory manifestations. Moreover, ubiquitination modification of CEBPB by constitutive photomorphogenesis protein 1 homolog (COP1) led to the degradation of CEBPB and inhibited inflammatory responses in macrophages. Upregulation of COP1 protected against SIMI in mice overexpressing CEBPB. Collectively, our findings demonstrated that COP1 protected the heart against SIMI through the ubiquitination modification of CEBPB, which might be a novel therapeutic approach in the future | ||
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