Possible changes in expression of chemotaxin LECT2 mRNA in mouse liver after concanavalin A-induced hepatic injury
Open accessAbstract
The functions of leukocyte-derived chemotaxin 2 (LECT2), a novel liver-specific protein, are not well defined, especially after hepatic injury. The changes in expression of LECT2 mRNA were investigated after concanavalin A (Con A)-induced hepatic injury in mice. Serum glutamate pyruvate transaminase (s-GPT) activity and the percentage of liver DNA fragmentation, an indicator of hepatic apoptosis, increased 8 h after intravenous administration of Con A (13 mg/kg). Expression of LECT2 mRNA was reduced from 8-24 h after injection of Con A, but was detected again 48 h after recovery from hepatic injury. Expression of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma mRNA was observed in liver 2 h after Con A injection. Z-Val-Ala-Asp(OMe)-CH2F (Z-VAD-FMK), a caspase inhibitor, was administered to mice to investigate whether LECT2 was involved in apoptosis of liver cells after Con A injection. Z-VAD-FMK inhibited s-GPT activity and DNA fragmentation in the liver 8 h after Con A-induced hepatic injury, but did not prevent the reduction of LECT2 mRNA, or induction of TNF-alpha and IFN-gamma mRNA expression. When the relation between expression of LECT2, TNF-alpha and IFN-gamma mRNAs was examined 8 h after Con A injection in wild-type or immunodeficient (nu-/nu-) mice, the increase in TNF-alpha and IFN-gamma mRNA expression was found to be closely related to a reduction in LECT2 mRNA expression. These results suggest that the reduction in expression of LECT2 mRNA is not directly involved in apoptosis and may be inversely related to the expression of TNF-alpha and/or IFN-gamma mRNA in the injured liver.
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LECT2 functions in liver regeneration, immune modulation, bone growth, neural development, glucose metabolism, metabolic syndrome, and cancer.
“LECT2 functions in liver regeneration, immune modulation, bone growth, neural development, glucose metabolism, metabolic syndrome, and cancer [[241], [242], [243], [244], [245], [246]].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [241]
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- Authors
- SEGAWA, Y., ITOKAZU, Y., INOUE, N., SAITO, T., & SUZUKI, K.
- Affiliations
- Zeria Pharmaceutical (Japan) (JP)
- National Institute of Infectious Diseases (JP)
- Venue
- Biological and Pharmaceutical Bulletin
- Publisher
- Pharmaceutical Society of Japan
- Published
- 2001
- Volume
- 24
- Issue
- 4
- Pages
- 425-428
- ISSN
- 0918-6158 (ISSN-L)
- 1347-5215
- OpenAlex
- W1990910530
- Cited by
- 22
- References
- 15
- Citations by year
- 2024: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 3
- FWCI
- 0.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological and Pharmaceutical Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- LECT2, concanavalin A-induced liver injury, hepatic apoptosis, TNF-α, interferon-gamma, caspase inhibition, z-VAD-fmk, alanine aminotransferase, immunodeficient nude mice, liver-specific gene expression
- MeSH terms
- Alanine Transaminase, Animals, Chemotactic Factors, Concanavalin A, Enzyme Inhibitors, Female, Interferon-gamma, Liver, Liver Function Tests, Mice, Inbred BALB C, RNA, Messenger, Protein Biosynthesis, Tumor Necrosis Factor-alpha, Blotting, Western, Intercellular Signaling Peptides and Proteins, Mice, DNA Fragmentation, Chemical and Drug Induced Liver Injury, Caspase Inhibitors
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