Oxidative stress induced lipocalin 2 gene expression: Addressing its expression under the harmful conditions
Journal of Radiation Research, ISSN: 1349-9157, Vol: 48, Issue: 1, Page: 39-44
2007
- 144Citations
- 53Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations144
- Citation Indexes144
- 144
- CrossRef89
- Captures53
- Readers53
- 53
Article Description
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 O. Interestingly, up-regulation of Lcn2 expression after HO 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.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33846888090&origin=inward; http://dx.doi.org/10.1269/jrr.06057; http://www.ncbi.nlm.nih.gov/pubmed/17229997; https://academic.oup.com/jrr/article-lookup/doi/10.1269/jrr.06057; https://dx.doi.org/10.1269/jrr.06057; https://academic.oup.com/jrr/article/48/1/39/925722
Oxford University Press (OUP)
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