title: Possible changes in expression of chemotaxin LECT2 mRNA in mouse liver after concanavalin A-induced hepatic injury.
abstract: 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.
authors: Zeria Pharmaceutical Co., Ltd., Ohsato-gun, Saitama, Japan. ken-yakuri@zeria.co.jp
authors: Y
authors: Y
authors: Segawa
authors: Y
authors: Y
authors: Itokazu
authors: N
authors: N
authors: Inoue
authors: T
authors: T
authors: Saito
authors: K
authors: K
authors: Suzuki
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D015153:Blotting, Western; D061945:Caspase Inhibitors; D056486:Chemical and Drug Induced Liver Injury / Q000378:metabolism*; D002630:Chemotactic Factors / Q000096:biosynthesis*; D003208:Concanavalin A / Q000633:toxicity*; D053938:DNA Fragmentation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D036341:Intercellular Signaling Peptides and Proteins; D007371:Interferon-gamma / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism*; D008111:Liver Function Tests; D051379:Mice; D008807:Mice, Inbred BALB C; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D061945:Caspase Inhibitors; D002630:Chemotactic Factors; D004791:Enzyme Inhibitors; D036341:Intercellular Signaling Peptides and Proteins; C491213:Lect2 protein, mouse; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D003208:Concanavalin A; D007371:Interferon-gamma; D000410:Alanine Transaminase