The danger signal interferon-induced protein 35 (IFP35) mediates acetaminophen-induced liver injury
Copyright © 2022 Elsevier Inc. All rights reserved..
Acute liver injury caused by overdose usage of acetaminophen (APAP) is an intractable clinical problem. Necrotic hepatocytes release large amounts of intracellular components including damage-associated molecular patterns (DAMPs) which contribute to liver failure and may serve as therapeutic targets. However, the pathogenic mechanisms of DAMPs in APAP-induced liver injury (AILI) are remain largely uncovered. Here, we found that a recently identified DAMP, interferon-induced protein 35 (IFP35), is involved in the early phase of AILI. Our data demonstrated that although the expression level of IFP35 is not significantly increased in either patients or mice with AILI, it is released from necrotic hepatocytes. Within 24 h post APAP injection, mice lacking Ifp35 are resistant to APAP-induced toxicity, and induce less inflammatory response than that of wild-type mice, including reduced AST/ALT level, pro-inflammatory cytokines production and neutrophils infiltration. More importantly, antibody of IFP35 reduces the expression level of inflammatory factors and chemokines. This study brings new knowledge into the pathogenic mechanism of AILI.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:621 |
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| Enthalten in: |
Biochemical and biophysical research communications - 621(2022) vom: 17. Sept., Seite 25-31 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Mao, Xiating [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 05.08.2022 Date Revised 09.08.2022 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.bbrc.2022.06.086 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
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| 245 | 1 | 4 | |a The danger signal interferon-induced protein 35 (IFP35) mediates acetaminophen-induced liver injury |
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| 520 | |a Copyright © 2022 Elsevier Inc. All rights reserved. | ||
| 520 | |a Acute liver injury caused by overdose usage of acetaminophen (APAP) is an intractable clinical problem. Necrotic hepatocytes release large amounts of intracellular components including damage-associated molecular patterns (DAMPs) which contribute to liver failure and may serve as therapeutic targets. However, the pathogenic mechanisms of DAMPs in APAP-induced liver injury (AILI) are remain largely uncovered. Here, we found that a recently identified DAMP, interferon-induced protein 35 (IFP35), is involved in the early phase of AILI. Our data demonstrated that although the expression level of IFP35 is not significantly increased in either patients or mice with AILI, it is released from necrotic hepatocytes. Within 24 h post APAP injection, mice lacking Ifp35 are resistant to APAP-induced toxicity, and induce less inflammatory response than that of wild-type mice, including reduced AST/ALT level, pro-inflammatory cytokines production and neutrophils infiltration. More importantly, antibody of IFP35 reduces the expression level of inflammatory factors and chemokines. This study brings new knowledge into the pathogenic mechanism of AILI | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Acetaminophen | |
| 650 | 4 | |a Acute liver injury | |
| 650 | 4 | |a Aseptic inflammatory | |
| 650 | 4 | |a Damage-associated molecular pattern | |
| 650 | 4 | |a Neutrophils | |
| 650 | 7 | |a IFP35 protein, mouse |2 NLM | |
| 650 | 7 | |a Intracellular Signaling Peptides and Proteins |2 NLM | |
| 650 | 7 | |a Acetaminophen |2 NLM | |
| 650 | 7 | |a 362O9ITL9D |2 NLM | |
| 650 | 7 | |a Interferons |2 NLM | |
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| 700 | 1 | |a Wu, Danning |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Na |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jingjing |e verfasserin |4 aut | |
| 700 | 1 | |a Zeng, Jinhua |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Zhiqiang |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yingfang |e verfasserin |4 aut | |
| 700 | 1 | |a Liang, Huanhuan |e verfasserin |4 aut | |
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