Roudkenar Mehryar Habibi, Kuwahara Yoshikazu, Baba Taisuke, Roushandeh Amaneh Mohammadi, Ebishima Shigeko, Abe Shinya, Ohkubo Yasuhito, Fukumoto Manabu
Department of Pathology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
J Radiat Res. 2007 Jan;48(1):39-44. doi: 10.1269/jrr.06057. Epub 2007 Jan 16.
Lipocalin 2 (Lcn2, NGAL) is a member of the lipocalin superfamily with diverse functions such as the transport of fatty acids and the induction of apoptosis. Previous reports indicated that expression of Lcn2 is induced under harmful conditions. However, the mechanisms of the induction of Lcn2 expression remain to be elucidated. In this report, we intended to identify the factor or factors that induce Lcn2 expression. Up-regulation of Lcn2 expression after X-ray exposure was detected in the heart, the kidney and especially in the liver. Primary culture of liver component cells revealed that this up-regulation in the liver was induced in hepatocytes. Up-regulation of Lcn2 expression was also detected in HepG2 cells after the administration of X-rays or H(2)O(2). Interestingly, up-regulation of Lcn2 expression after H(2)O(2) treatment was canceled by the addition of the anti-oxidants, dimethylsulfoxide or cysteamine. These results strongly suggest that Lcn2 expression is induced by reactive oxygen species. Therefore, Lcn2 could be a useful biomarker to identify oxidative stress both in vitro and in vivo.
脂钙蛋白2（Lcn2，NGAL）是脂钙蛋白超家族的成员，具有多种功能，如脂肪酸转运和诱导细胞凋亡。先前的报道表明，Lcn2的表达在有害条件下被诱导。然而，Lcn2表达的诱导机制仍有待阐明。在本报告中，我们旨在确定诱导Lcn2表达的一个或多个因素。在心脏、肾脏尤其是肝脏中检测到X射线照射后Lcn2表达上调。肝脏组成细胞的原代培养显示，肝脏中的这种上调是在肝细胞中诱导的。在给予X射线或H₂O₂后，HepG2细胞中也检测到Lcn2表达上调。有趣的是，添加抗氧化剂二甲基亚砜或半胱胺可消除H₂O₂处理后Lcn2表达的上调。这些结果强烈表明，Lcn2表达是由活性氧诱导的。因此，Lcn2可能是一种在体外和体内识别氧化应激的有用生物标志物。
