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

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 fai...

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Autores principales:	Mengjing Li, Tao Ling, Fengmeng Teng, Chao Hu, Zhongping Su, Chen Zhang, Xiang Li, Ting Zhao, Xianmin Mu, Yingchang Li, Jinshun Pan, Qiang You
Formato:	article
Lenguaje:	EN
Publicado:	Nature Publishing Group 2021
Materias:	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Cytology QH573-671
Acceso en línea:	https://doaj.org/article/ca6ed55cf1f44af9be5ac7940ab9efec
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spelling	oai:doaj.org-article:ca6ed55cf1f44af9be5ac7940ab9efec2021-11-14T12:12:37ZCD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway10.1038/s41420-021-00742-32058-7716https://doaj.org/article/ca6ed55cf1f44af9be5ac7940ab9efec2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41420-021-00742-3https://doaj.org/toc/2058-7716Abstract 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.Mengjing LiTao LingFengmeng TengChao HuZhongping SuChen ZhangXiang LiTing ZhaoXianmin MuYingchang LiJinshun PanQiang YouNature Publishing GrouparticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282CytologyQH573-671ENCell Death Discovery, Vol 7, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Cytology QH573-671
spellingShingle	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Cytology QH573-671 Mengjing Li Tao Ling Fengmeng Teng Chao Hu Zhongping Su Chen Zhang Xiang Li Ting Zhao Xianmin Mu Yingchang Li Jinshun Pan Qiang You CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
description	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.
format	article
author	Mengjing Li Tao Ling Fengmeng Teng Chao Hu Zhongping Su Chen Zhang Xiang Li Ting Zhao Xianmin Mu Yingchang Li Jinshun Pan Qiang You
author_facet	Mengjing Li Tao Ling Fengmeng Teng Chao Hu Zhongping Su Chen Zhang Xiang Li Ting Zhao Xianmin Mu Yingchang Li Jinshun Pan Qiang You
author_sort	Mengjing Li
title	CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
title_short	CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
title_full	CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
title_fullStr	CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
title_full_unstemmed	CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway
title_sort	cd5l deficiency attenuate acetaminophen-induced liver damage in mice via regulation of jnk and erk signaling pathway
publisher	Nature Publishing Group
publishDate	2021
url	https://doaj.org/article/ca6ed55cf1f44af9be5ac7940ab9efec
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CD5L deficiency attenuate acetaminophen-induced liver damage in mice via regulation of JNK and ERK signaling pathway

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