文章基本信息

标题：Possible Changes in Expression of Chemotaxin LECT2 mRNA in Mouse Liver after Concanavalin A-Induced Hepatic Injury
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作者：Yoshihide SEGAWA ; Yoshihiko ITOKAZU ; Naonori INOUE 等
期刊名称：Biological and Pharmaceutical Bulletin
印刷版ISSN：0918-6158
电子版ISSN：1347-5215
出版年度：2001
卷号：24
期号：4
页码：425-428
DOI：10.1248/bpb.24.425
出版社：The Pharmaceutical Society of Japan
摘要：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)-α and interferon (IFN)-γ 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-α and IFN-γ mRNA expression. When the relation between expression of LECT2, TNF-α and IFN-γ mRNAs was examined 8 h after Con A injection in wild-type or immunodeficient (nu^-/nu^-) mice, the increase in TNF-α and IFN-γ 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-α and/or IFN-γ mRNA in the injured liver.
关键词：leukocyte-derived chemotaxin 2;Con A-induced hepatic injury;apoptosis;LECT2;TNF-α and IFN-γ mRNA