Department of Hematology and Rheumatology, Tohoku University Graduate School, Sendai, Japan ; Molecular Hematology/Oncology, Tohoku University Graduate School, Sendai, Japan.
PLoS One. 2013 Sep 27;8(9):e75568. doi: 10.1371/journal.pone.0075568. eCollection 2013.
Hepcidin is the principal iron regulatory hormone, controlling the systemic absorption and remobilization of iron from intracellular stores. The expression of the hepcidin gene, HAMP, is increased in patients with anemia of chronic disease. Previously, the synthetic compound K7174 was identified through chemical screening as a novel inhibitor of the adhesion of monocytes to cytokine-stimulated endothelial cells. K7174 also ameliorated anemia induced by inflammatory cytokines in mice, which suggests a possible involvement of hepcidin regulation. The present study was performed to assess the impact of K7174 on hepcidin expression in a human hematoma cell line and in mice in vivo. We first demonstrated that K7174 treatment in HepG2 cells significantly decreased HAMP expression. Then, we conducted microarray analysis to determine the molecular mechanism by which K7174 inhibits HAMP expression. Transcriptional profiling confirmed the downregulation of HAMP. Surprisingly, we found that K7174 strongly induced GDF15, known as a negative regulator of HAMP expression. Western blotting analysis as well as ELISA confirmed the induction of GDF15 by K7174 treatment. Furthermore, K7174-mediated HAMP suppression was rescued by the silencing of GDF15 expression. Interestingly, we found that K7174 also upregulates CEBPB. Promoter analysis and chromatin immunoprecipitation analysis revealed that CEBPB could contribute to K7174-mediated transcriptional activation of GDF15. Subsequently, we also examined whether K7174 inhibits hepcidin expression in mice. Quantitative RT-PCR analysis with liver samples from K7174-treated mice demonstrated significant upregulation of Gdf15 and downregulation of Hamp expression, as compared to control mice. Furthermore, serum hepcidin concentration was also significantly decreased in K7174-treated mice. In conclusion, K7174 inhibits hepcidin expression partly by inducing GDF15. K-7174 may be a potential therapeutic option to treat anemia of chronic disease.
亚铁调素是主要的铁调节激素,控制着细胞内储存铁的系统性吸收和再动员。在慢性疾病贫血患者中,亚铁调素基因 HAMP 的表达增加。此前,通过化学筛选发现合成化合物 K7174 是一种新型的单核细胞与细胞因子刺激的内皮细胞黏附抑制剂。K7174 还改善了炎症细胞因子诱导的小鼠贫血,这表明铁调素调节可能参与其中。本研究旨在评估 K7174 对人血肿细胞系和体内小鼠中铁调素表达的影响。我们首先证明 K7174 处理 HepG2 细胞可显著降低 HAMP 表达。然后,我们进行了微阵列分析,以确定 K7174 抑制 HAMP 表达的分子机制。转录谱分析证实了 HAMP 的下调。令人惊讶的是,我们发现 K7174 强烈诱导了 GDF15,GDF15 是 HAMP 表达的负调节因子。Western blot 分析和 ELISA 证实了 K7174 处理诱导 GDF15 的表达。此外,GDF15 表达沉默可挽救 K7174 介导的 HAMP 抑制。有趣的是,我们发现 K7174 还上调了 CEBPB。启动子分析和染色质免疫沉淀分析表明,CEBPB 可能有助于 K7174 介导的 GDF15 转录激活。随后,我们还检查了 K7174 是否抑制了小鼠中的铁调素表达。用 K7174 处理的小鼠肝组织进行定量 RT-PCR 分析显示,与对照组小鼠相比,Gdf15 显著上调,Hamp 表达下调。此外,K7174 处理的小鼠血清铁调素浓度也显著降低。总之,K7174 通过诱导 GDF15 抑制铁调素表达。K-7174 可能是治疗慢性疾病贫血的一种潜在治疗选择。