Immenschuh S, Nell C, Iwahara S, Katz N, Muller-Eberhard U
Institut für Klinische Chemie u. Pathobiochemie, Justus Liebig Universität Giessen, Germany.
Biochem Biophys Res Commun. 1997 Feb 24;231(3):667-70. doi: 10.1006/bbrc.1997.6166.
Heme-binding protein 23 kDa (HBP23) belongs to the antioxidant family of peroxiredoxins and binds heme with high affinity. In vivo treatment of rats with heme induced expression of HBP23 mRNA levels in liver coordinately with that of the heme degrading enzyme heme oxygenase-1 (HO-1). In primary rat hepatocyte cultures Sn-, Co-, and Zn-metalloprotoporphyrin as well as the heme precursor protoporphyrin IX increased the HBP23 mRNA expression to a level similar to that elicited by heme. Heme-dependent induction of HBP23 mRNA was prevented by pretreatment with actinomycin D, indicating a transcriptional mechanism of gene induction. The results suggest that the coordinate gene regulation pattern of HBP23 and HO-1 plays a physiological role against oxidative stress.
23 kDa血红素结合蛋白（HBP23）属于过氧化物酶抗氧化家族，能以高亲和力结合血红素。在体内用血红素处理大鼠，可诱导肝脏中HBP23 mRNA水平与血红素降解酶血红素加氧酶-1（HO-1）的表达协同上调。在原代大鼠肝细胞培养物中，锡、钴和锌金属原卟啉以及血红素前体原卟啉IX可将HBP23 mRNA表达增加至与血红素诱导水平相似。用放线菌素D预处理可阻止血红素依赖性HBP23 mRNA的诱导，表明存在基因诱导的转录机制。结果表明，HBP23和HO-1的协同基因调控模式在对抗氧化应激中发挥生理作用。
