CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway

CD5 molecule like (CD5L), a member of the scavenger receptor cysteine-rich domain superfamily, plays a critical role in immune homeostasis and inflammatory disease. Acetaminophen (APAP) is a safe and effective antipyretic analgesic. However, overdose may cause liver damage or even liver failure. APA...

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Published in:Cell death discovery 2021-11, Vol.7 (1), p.342-11, Article 342
Main Authors: Li, Mengjing, Ling, Tao, Teng, Fengmeng, Hu, Chao, Su, Zhongping, Zhang, Chen, Li, Xiang, Zhao, Ting, Mu, Xianmin, Li, Yingchang, Pan, Jinshun, You, Qiang
Format: Article
Language:English
Subjects:
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Acetaminophen
Alanine
Alanine transaminase
Analgesics
Apoptosis
Biochemistry
Biomedical and Life Sciences
c-Jun protein
CD5 antigen
Cell Biology
Cell Cycle Analysis
Cell death
Cell permeability
Cytokines
Endothelial cells
Extracellular signal-regulated kinase
Hepatotoxicity
Homeostasis
Inflammatory diseases
JNK protein
Life Sciences
Liver
Liver diseases
Overdose
Phosphorylation
Scavenger receptors
Signal transduction
Stem Cells
Therapeutic targets
Transaminase
Transcription factors
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Summary:CD5 molecule like (CD5L), a member of the scavenger receptor cysteine-rich domain superfamily, plays a critical role in immune homeostasis and inflammatory disease. Acetaminophen (APAP) is a safe and effective antipyretic analgesic. However, overdose may cause liver damage or even liver failure. APAP hepatotoxicity is characterized by extensive necrotic cell death and a sterile inflammatory response, in which the role of CD5L remains to be investigated. In this study, we found that the expression of CD5L was increased in the livers of mice after APAP overdose. Furthermore, CD5L deficiency reduced the increase of alanine transaminase (ALT) level, histopathologic lesion area, c-Jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK) phosphorylation level, Transferase-Mediated dUTP Nick End-Labeling positive (TUNEL + ) cells proportion, vascular endothelial cell permeability and release of inflammatory cytokines induced by excess APAP. Therefore, our findings reveal that CD5L may be a potential therapeutic target for prevention and treatment of APAP-induced liver injury.
ISSN:2058-7716
2058-7716
DOI:10.1038/s41420-021-00742-3