Department of Pharmaceutics, Amgen, Thousand Oaks, California 91320, USA.
Biophys J. 2009 Jan;96(1):199-208. doi: 10.1016/j.bpj.2008.10.002.
The complex, multistep aggregation kinetic and structural behavior of human recombinant interleukin-1 receptor antagonist (IL-1ra) was revealed and characterized by spectral probes and techniques. At a certain range of protein concentration (12-27 mg/mL) and temperature (44-48 degrees C), two sequential aggregation kinetic transitions emerge, where the second transition is preceded by a lag phase and is associated with the main portion of the aggregated protein. Each kinetic transition is linked to a different type of aggregate population, referred to as type I and type II. The aggregate populations, isolated at a series of time points and analyzed by Fourier-transform infrared spectroscopy, show consecutive protein structural changes, from intramolecular (type I) to intermolecular (type II) beta-sheet formation. The early type I protein spectral change resembles that seen for IL-1ra in the crystalline state. Moreover, Fourier-transform infrared data demonstrate that type I protein assembly alone can undergo a structural rearrangement and, consequently, convert to the type II aggregate. The aggregated protein structural changes are accompanied by the aggregate morphological changes, leading to a well-defined population of interacting spheres, as detected by scanning electron microscopy. A nucleation-driven IL-1ra aggregation pathway is proposed, and assumes two major activation energy barriers, where the second barrier is associated with the type I --> type II aggregate structural rearrangement that, in turn, serves as a pseudonucleus triggering the second kinetic event.
通过光谱探针和技术,揭示并表征了人重组白细胞介素-1 受体拮抗剂(IL-1ra)的复杂、多步聚集动力学和结构行为。在一定的蛋白质浓度(12-27mg/mL)和温度(44-48°C)范围内,出现了两个连续的聚集动力学转变,其中第二个转变之前有一个滞后阶段,与大部分聚集的蛋白质有关。每个动力学转变都与不同类型的聚集物群体有关,分别称为 I 型和 II 型。在一系列时间点分离聚集物群体,并通过傅里叶变换红外光谱进行分析,显示出连续的蛋白质结构变化,从分子内(I 型)到分子间(II 型)β-折叠形成。早期的 I 型蛋白质光谱变化类似于 IL-1ra 在结晶状态下的变化。此外,傅里叶变换红外数据表明,仅 I 型蛋白质组装就可以进行结构重排,并因此转化为 II 型聚集物。聚集蛋白结构的变化伴随着聚集形态的变化,导致相互作用球体的明确群体,如扫描电子显微镜检测到的那样。提出了一种由成核驱动的 IL-1ra 聚集途径,并假设存在两个主要的活化能障碍,其中第二个障碍与 I 型到 II 型聚集结构重排有关,这反过来又作为触发第二个动力学事件的伪核。