Oxidative Stress Induced Lipocalin 2 Gene Expression: Addressing its Expression under the Harmful Conditions
Author(s) -
Mehryar Habibi Roudkenar,
Yoshikazu Kuwahara,
Taisuke Baba,
Amaneh Mohammadi Roushandeh,
Shigeko Ebishima,
Shinya Abe,
Yasuhito Ohkubo,
Manabu Fukumoto
Publication year - 2007
Publication title -
journal of radiation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.643
H-Index - 60
eISSN - 1349-9157
pISSN - 0449-3060
DOI - 10.1269/jrr.06057
Subject(s) - lipocalin , oxidative stress , reactive oxygen species , apoptosis , gene expression , microbiology and biotechnology , biology , gene , in vitro , regulation of gene expression , in vivo , keap1 , biomarker , chemistry , biochemistry , transcription factor , genetics
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.
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