Laboratory of Molecular Neurobiology and Functional Neuroproteomics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland.
J Biol Chem. 2010 Aug 20;285(34):26581-98. doi: 10.1074/jbc.M110.113951. Epub 2010 Jun 1.
Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, is considered an attractive therapeutic target in multiple inflammatory and autoimmune disorders. In addition to its known biologic activities, MIF can also function as a tautomerase. Several small molecules have been reported to be effective inhibitors of MIF tautomerase activity in vitro. Herein we employed a robust activity-based assay to identify different classes of novel inhibitors of the catalytic and biological activities of MIF. Several novel chemical classes of inhibitors of the catalytic activity of MIF with IC(50) values in the range of 0.2-15.5 microm were identified and validated. The interaction site and mechanism of action of these inhibitors were defined using structure-activity studies and a battery of biochemical and biophysical methods. MIF inhibitors emerging from these studies could be divided into three categories based on their mechanism of action: 1) molecules that covalently modify the catalytic site at the N-terminal proline residue, Pro(1); 2) a novel class of catalytic site inhibitors; and finally 3) molecules that disrupt the trimeric structure of MIF. Importantly, all inhibitors demonstrated total inhibition of MIF-mediated glucocorticoid overriding and AKT phosphorylation, whereas ebselen, a trimer-disrupting inhibitor, additionally acted as a potent hyperagonist in MIF-mediated chemotactic migration. The identification of biologically active compounds with known toxicity, pharmacokinetic properties, and biological activities in vivo should accelerate the development of clinically relevant MIF inhibitors. Furthermore, the diversity of chemical structures and mechanisms of action of our inhibitors makes them ideal mechanistic probes for elucidating the structure-function relationships of MIF and to further determine the role of the oligomerization state and catalytic activity of MIF in regulating the function(s) of MIF in health and disease.
巨噬细胞移动抑制因子(MIF)是一种前炎性细胞因子,被认为是多种炎症和自身免疫性疾病有吸引力的治疗靶点。除了其已知的生物学活性外,MIF 还可以作为互变异构酶。已经报道了几种小分子可以有效地抑制 MIF 互变异构酶的体外活性。在此,我们采用了一种强大的基于活性的测定法来鉴定不同类别的新型 MIF 催化和生物学活性抑制剂。鉴定并验证了几种新型 MIF 催化活性抑制剂,其 IC50 值在 0.2-15.5 微米范围内。使用结构活性研究和一系列生化和生物物理方法确定了这些抑制剂的相互作用位点和作用机制。根据作用机制,从这些研究中出现的 MIF 抑制剂可以分为三类:1)共价修饰 N-端脯氨酸残基(Pro1)催化位点的分子;2)新型催化位点抑制剂;最后 3)破坏 MIF 三聚体结构的分子。重要的是,所有抑制剂均完全抑制 MIF 介导的糖皮质激素替代和 AKT 磷酸化,而三唑抑制剂 ebselen 除了作为 MIF 介导的趋化迁移的有效超激动剂外。具有已知毒性,药代动力学性质和体内生物学活性的生物活性化合物的鉴定应加速具有临床相关性的 MIF 抑制剂的开发。此外,我们抑制剂的化学结构和作用机制的多样性使它们成为阐明 MIF 的结构-功能关系的理想机制探针,并进一步确定 MIF 的寡聚状态和催化活性在调节 MIF 在健康和疾病中的功能方面的作用。