Expression of human carbonyl reductase 3 (CBR3; SDR21C2) is inducible by pro-inflammatory stimuli

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• 作者：Petra Malá ; tková ; ^a ; Bettina Ebert^b ; Vladimí ; r Wsó ; l^a ; Edmund Maser^b ; ^{maser@toxi.uni-kiel.de}
• 关键词：CBR3 ; carbonyl reductase 3 ; IL-1 ; interleukin-1 ; LPS ; lipopolysaccharides ; NF魏B ; nuclear-factor kappa-B ; qPCR ; quantitative real-time RT-PCR ; sqPCR ; semi-quantitative RT-PCR ; TNF-伪 ; tumor necrosis factor-伪
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：6 April, 2012
• 卷：420
• 期：2
• 页码：368-373
• 文件大小：570 K

摘要

Until today, the physiologic role of human carbonyl reductase 3 (CBR3; SDR21C2), a member of the short-chain dehydrogenase/reductase superfamily remains obscure. Since the transcriptional regulation is closely related to the function of a protein, elucidation of the regulation of CBR3 should help to understand its physiologic role. We recently identified CBR3 as a novel target gene of Nrf2, a cellular sensor of oxidative stress. In this study, we provide for the first time evidence that pro-inflammatory stimuli induce the expression of the CBR3 gene. Treatment of human cancer cells HT-29 (colon) and HepG2 (liver) with TNF-伪, IL-1尾, and LPS induced CBR3 expression differentially. While TNF-伪 (50 ng/ml) or IL-1尾 (1 and 10 ng/ml), induced CBR3 mRNA expression in HT-29 cells (up to 10-fold) and HepG2 cells (up to 20-fold), LPS activated the CBR3 gene only in HepG2 cells. Furthermore, overexpression of the NF魏B subunits p65 and p50 alone or in combination elevated CBR3 mRNA levels (3.9-fold) in HT-29 cells. According to our results, CBR3 is a novel target gene of inflammatory stimuli, and elucidation of its detailed role in inflammation deserves further investigation.