Hepatoma-derived growth factor participates in concanavalin A-induced hepatitis.


Journal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484

Informations de publication

Date de publication:
12 2020
Historique:
received: 06 03 2020
revised: 13 09 2020
accepted: 28 09 2020
pubmed: 17 10 2020
medline: 24 4 2021
entrez: 16 10 2020
Statut: ppublish

Résumé

Hepatitis is an important health problem worldwide. Novel molecular targets are in demand for detection and management of hepatitis. Hepatoma-derived growth factor (HDGF) has been delineated to participate in hepatic fibrosis and liver carcinogenesis. However, the relationship between hepatitis and HDGF remains unclear. This study aimed to elucidate the role of HDGF during hepatitis using concanavalin A (ConA)-induced hepatitis model. In cultured hepatocytes, ConA treatment-elicited HDGF upregulation at transcriptional level and promoted HDGF secretion while reducing intracellular HDGF protein level and cellular viability. Similarly, mice receiving ConA administration exhibited reduced hepatic HDGF expression and elevated circulating HDGF level, which was positively correlated with serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. By using HDGF knockout (KO) mice, it was found the ConA-evoked cell death was prominently alleviated in KO compared with control. Besides, it was delineated HDGF ablation conferred protection by suppressing the ConA-induced neutrophils recruitment in livers. Above all, the ConA-mediated activation of tumor necrosis factor-α (TNF-α)/interleukin-1β (IL-1β)/interleukin-6 (IL-6)/cyclooxygenase-2 (COX-2) inflammatory signaling was significantly abrogated in KO mice. Treatment with recombinant HDGF (rHDGF) dose-dependently stimulated the expression of TNF-α/IL-1β/IL-6/COX-2 in hepatocytes, further supporting the pro-inflammatory function of HDGF. Finally, application of HDGF antibody not only attenuated the ConA-mediated inflammatory cascade in hepatocytes, but also ameliorated the ConA-induced hepatic necrosis and AST elevation in mice. In summary, HDGF participates in ConA-induced hepatitis via neutrophils recruitment and may constitute a therapeutic target for acute hepatitis.

Identifiants

pubmed: 33063394
doi: 10.1096/fj.202000511RR
doi:

Substances chimiques

Intercellular Signaling Peptides and Proteins 0
Interleukin-1beta 0
Interleukin-6 0
Tumor Necrosis Factor-alpha 0
hepatoma-derived growth factor 0
Concanavalin A 11028-71-0
Aspartate Aminotransferases EC 2.6.1.1
Alanine Transaminase EC 2.6.1.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

16163-16178

Informations de copyright

© 2020 Federation of American Societies for Experimental Biology.

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Auteurs

E-Ming Wang (EM)

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Tsung-Hui Hu (TH)

Division of Hepato-Gastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Chao-Cheng Huang (CC)

Biobank and Tissue Bank, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Department of Pathology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Yi-Chen Chang (YC)

Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University and Academia Sinica, Kaohsiung, Taiwan.

Shih-Ming Yang (SM)

Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.

Shih-Tsung Huang (ST)

Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University and Academia Sinica, Kaohsiung, Taiwan.
LabTurbo Biotech Corporation, Taipei, Taiwan.

Jian-Ching Wu (JC)

Biobank and Tissue Bank, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Department of Pathology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Yi-Ling Ma (YL)

Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Hoi-Hung Chan (HH)

Division of Gastroenterology, Department of Medicine, Conde S. Januário Hospital, Macau, China.

Li-Feng Liu (LF)

Department of Biological Science & Technology, I-Shou University, Kaohsiung, Taiwan.

Wen-Bin Lu (WB)

Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.

Mei-Lang Kung (ML)

Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Zhi-Hong Wen (ZH)

Department of Marine Biotechnology and Resources, Asia-Pacific Ocean Research Center, National Sun Yat-sen University, Kaohsiung, Taiwan.

Jui-Chu Wang (JC)

Department of Pathology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Chou-Yuan Ko (CY)

Department of Gastroenterology, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.

Wei-Lun Tsai (WL)

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Tian-Huei Chu (TH)

Biobank and Tissue Bank, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.

Ming-Hong Tai (MH)

Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
Doctoral Degree Program in Marine Biotechnology, National Sun Yat-sen University and Academia Sinica, Kaohsiung, Taiwan.
Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
Center for Neuroscience, National Sun Yat-sen University, Kaohsiung, Taiwan.
Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.

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