Cell Death Discovery (Nov 2021)

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

  • Mengjing Li,
  • Tao Ling,
  • Fengmeng Teng,
  • Chao Hu,
  • Zhongping Su,
  • Chen Zhang,
  • Xiang Li,
  • Ting Zhao,
  • Xianmin Mu,
  • Yingchang Li,
  • Jinshun Pan,
  • Qiang You

DOI
https://doi.org/10.1038/s41420-021-00742-3
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 11

Abstract

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Abstract 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.